sort by

116 publications mentioning hsa-mir-139 (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-139. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 366
Other miRNAs from this paper: hsa-mir-21
Analysis of the mRNA expression profiles revealed 354 differentially expressed genes, 89 upregulated genes, and 265 downregulated genes between miR-139-5p mimic -treated cells and NCs. [score:11]
As shown in Figure 6A, EC109 showed the lowest expression of miR-139-5p, and CaEs-17 had the highest expression, whereas NR5A2 showed the highest expression in KYSE-150 but the lowest expression level in EC9706. [score:9]
Given that miR-139-5p has been established to regulate NR5A2 expression by binding with the conserved site of NR5A2 in the 3′UTR region, the changes in NR5A2 expression levels are related to the expression changes in miR-139-5p, which was confirmed with four esophageal cancer cell lines. [score:8]
Eighty-nine upregulated (ratio>2) and 265 downregulated mRNAs (ratio<0.5) were identified from miR-139-5p mimic -treated cells relative to NC cells (Table S1). [score:7]
Further analysis using TargetScan Release 6.2 predicted multiple miRNA target binding sites in the 3′UTR sequence of NR5A2, which meets the R-squared value of Pearson correlation analysis that showed the contribution of miR-139-5p to NR5A2 expression only accounted for approximately 8% in esophageal cancer patients. [score:7]
Moreover, the potential mRNA target of miR-139-5p, nuclear receptor subfamily 5, group A, member 2 (NR5A2), which induces cell proliferation through the concomitant induction of cyclin D1 and E1 and promotes cancer invasion through the remo deling of the actin cytoskeleton and E-cadherin cleavage in cancer development and metastasis [17], [18], [19], [20], [21], was identified using 3′UTR luciferase reporter assay and correlation analysis with miR-139-5p expression in a population study, which provides insight into the mechanisms underlying miRNA deregulation in esophageal cancer. [score:6]
Downregulation of miR-139-5p expression associated with a high risk for ESCC. [score:6]
Thus, the upregulation of miR-139-5p may induce important cellular changes by targeting specific genes. [score:6]
In this study, a significant negative correlation was found between miR-139-5p and NR5A2 expression in tumor tissues and in tissues adjacent to tumors, which suggests that miR-139-5p could affect oncogenic NR5A2 expression and is involved in the development and lymph node metastasis of esophageal cancer. [score:6]
Upregulated miR-139-5p Expression Arrests Cells in G0/G1 Phase. [score:6]
The results indicate that miR-139-5p suppressed NR5A2 expression, acting as a post-transcriptional repressor. [score:5]
Hence, a correlation analysis between the miR-139-5p expression and NR5A2 expression was performed in four ESCC cell lines except for KYSE-150. [score:5]
miR-139-5p Suppresses NR5A2 Expression by Binding to 3′UTR Sequence. [score:5]
Nuclear receptor subfamily 5, group A, member 2 (NR5A2) was predicted as a candidate target of miR-139-5p by the online TargetScan release 6.0 software (http://www. [score:5]
NR5A2 was identified as a potential miR-139-5p target owing to the conserved miR-139-5p binding site in the 3′UTR sequence of NR5A2 based on the prediction of TargetScan software. [score:5]
miR-139-5p was found to suppress cell proliferation and invasive capability of esophageal carcinoma cells and induce cell cycle arrest in the G0/G1 phase and in the late apoptosis of cancer cells by targeting oncogenic NR5A2. [score:5]
Nuclear receptor subfamily 5, group A, member 2 (NR5A2), a gene associated with cell cycle and cancer invasion, was predicted to harbor an 8-mer site that matches the complementary sequence of the miR-139-5p seed region based on a miRNA target prediction tool (TargetScan Release 6.0). [score:5]
The results suggest that miR-139-5p could suppress NR5A2 expression by binding to specific 3′UTR sequence. [score:5]
Overexpression of miR-139-5p Suppresses Cell Migratory Activity and Cell Invasiveness in vitro. [score:5]
The results revealed that the overexpression of miR-139-5p significantly suppressed the cell proliferation rate of EC109 cells (P<0.01). [score:5]
The experiments demonstrated the tumor suppressive features of miR-139-5p at the phenotype level, including its involvement in cell proliferation, cell cycle arrest, and cancer invasion, which were identified from the expression array at the gene level. [score:5]
The genomic expression level of total RNA samples from cells transfected with miR-139-5p mimic or NC was detected using Roche NimbleGen expression microarray. [score:5]
The result showed that miR-139-5p over -expression significantly suppressed cell migration both at 24 h and 48 h after wounding. [score:5]
Furthermore, the correlation analysis results from tumor tissues shows a relationship during the physiological lower expression of miR-139-5p, whereas the results from adjacent normal tissues show a relationship during the physiological higher expression of miR-139-5p. [score:5]
In summary, miR-139-5p was identified as a tumor suppressor gene associated with the risk for esophageal cancer, and a novel mechanism of regulation of NR5A2 protein by miR-139-5p was reported. [score:4]
The results indicate that as the downstream genes regulated by NR5A2, cyclin E1 and MMP9 respectively participated in the cell cycle arrest and invasive suppression induced by miR-139-5p. [score:4]
Luciferase reporter assay indicates that miR-139-5p could suppress NR5A2 expression by binding to specific 3′UTR sequences. [score:4]
A recent study reported that the downregulation of miR-139-5p in hepatocelluar carcinoma (HCC) was significantly associated with poor prognosis of patients and identified features of metastatic tumors, including venous invasion, microsatellite formation, absence of tumor encapsulation, and reduced differentiation [23]. [score:4]
Considering that miR-139-5p regulation of NR5A2 both in tumor tissues and in adjacent normal tissues operate under the same mechanism, the correlation of miR-139-5p and NR5A2 expression in tumor tissues would be similar to that in adjacent normal tissues. [score:4]
The present study demonstrated that miR-139-5p downregulates NR5A2 protein and mRNA levels and acts as a post-transcriptional repressor by binding to specific 3′UTR sequences in the NR5A2 transcript. [score:4]
The results suggest that miR-139-5p functions as a tumor-suppressor gene involved in esophageal cancer development. [score:4]
Cyclin E1 and MMP9 expression levels were reduced, indicating that these two downstream genes are regulated by NR5A2 and are suggested to participate in neoplasm proliferation and invasive process induced by miR-139-5p, respectively. [score:4]
ANOVA analysis indicated that the miR-139-5p mimic significantly inhibited the expression of wild 3′UTR constructs of NR5A2 (P<0.05) compared with other treatments. [score:4]
Kano et al. [13] identified the downregulation of miR-139-5p in ESCC tissues with a fold change of 0.175 by miRNA microarray. [score:4]
In this study, the relationship between miR-139-5p expression and the development of esophageal cancer was further validated in 106 pairs of esophageal cancer tissues and adjacent normal tissues. [score:4]
According to molecular and cellular functions, 24 of molecules involved in cellular growth and proliferation process were directly or indirectly regulated by miR-139-5p (P = 3.73E-03), whereas 13 and 12 of the molecules were respectively associated with cell death and cell cycle progression (P = 2.77E-03 and 3.66E-03). [score:4]
0077068.g005 Figure 5 A shows relative expression of NR5A2 in EC109 cells treated with miR-139-5p mimic or negative control normalized against β-actin using quantitative real time RT-PCR analysis. [score:3]
miR-139-5p Suppresses Cell Proliferation Ability in vitro. [score:3]
This study suggests that miR-139-5p suppresses growth and invasiveness in human ESCC by acting as a post-transcriptional repressor. [score:3]
Ingenuity pathway analysis (IPA) was performed to determine the biological functions that could be influenced by the overexpressed miR-139-5p in the EC109 cell line with the identified transcripts. [score:3]
A shows the relative expression of miR-139-5p and NR5A2 in five ESCC cell lines. [score:3]
0077068.g001 Figure 1 The top interactional network was identified by the Ingenuity Pathway Analysis software as significant function association of differentially expressed genes following introduction of miR-139-5p mimic. [score:3]
B shows the scatter plot of miR-139-5p and NR5A2 expression in ESCC patients. [score:3]
The results imply that miR-139-5p not only affects cell migratory activity, but also suppresses the invasive capability of EC109 cells. [score:3]
Association of NR5A2 mRNA Level with miR-139-5p Expression in ESCC Cell Lines and Esophageal Tissues. [score:3]
Table S2 Top 10 networks and functions of the differentially expressed transcripts influenced by miR-139-5p mimic in EC109 cells. [score:3]
Association of miR-139-5p and target gene NR5A2 in ESCC cell lines and ESCC patients. [score:3]
Table S1 The differentially expressed transcripts influenced by miR-139-5p mimic in EC109 cells. [score:3]
Consistent with the results from previous studies, the expression of miR-139-5p was found to be significantly reduced in esophageal cancer tissues, thereby implicating its tumorigenic relevance in multiple cancer types [14], [15], [16]. [score:3]
Blue bar represents the relative expression of miR-139-5p normalized against U6 in five ESCC cell lines. [score:3]
The results reveal that miR-139-5p overexpression induced the late apoptosis of EC109 cells. [score:3]
A shows relative expression of NR5A2 in EC109 cells treated with miR-139-5p mimic or negative control normalized against β-actin using quantitative real time RT-PCR analysis. [score:3]
Meanwhile, the reduced expression of miR-139-5p in tumor patients was supposed to be linked with lymph node metastases. [score:3]
The relationship between miR-139-5p and NR5A2 expression was analyzed using the Pearson correlation. [score:3]
The results show that miR-139-5p can suppress cell proliferation capability and participate in the retardation of G1/S phase transition during cell cycle progression. [score:3]
Fold changes in gene expression were determined with the normalized signal intensities of probes from miR-139-5p mimic treatment divided by the signal intensities from NC treatment. [score:3]
With the log-transformed relative expression data from tumor tissues and tissues adjacent to tumor, the Pearson correlation analysis showed a significantly negative correlation between miR-139-5p and NR5A2, as shown in Figure 6B (R = −0.284, P = 0.0002). [score:3]
The tumor-suppressive features of miR-139-5p in vitro, including cell proliferation and cell cycle involvement, migratory activity and invasion, as well as apoptosis, were then explored. [score:3]
Correlation analysis of the miR-139-5p expression and NR5A2 showed moderate correlation in four ESCC cell lines except for KYSE-150 (R = -0.398 for NR5A2 mRNA, and R = −0.370 for NR5A2 protein, respectively). [score:3]
The mixed sample set, including tumor tissues (diamond) and adjacent normal tissues (square) from ESCC patients, showed a significantly negative correlation between miR-139-5p and NR5A2 expression (R = −0.284, P = 0.0002). [score:3]
Genome-wide Transcription Network Analysis Affected by Overexpressed miR-139-5p. [score:3]
The correlation of miR-139-5p and NR5A2 expression in esophageal tissues was analyzed using Pearson correlation. [score:3]
0077068.g006 Figure 6 A shows the relative expression of miR-139-5p and NR5A2 in five ESCC cell lines. [score:3]
Pearson correlation was used to analyze the relationship between miR-139-5p and NR5A2 expression. [score:3]
Conditional logistic regression analysis revealed that reduced miR-139-5p expression was highly associated with increased risk for esophageal cancer (OR = 2.024). [score:3]
The top interactional network was identified by the Ingenuity Pathway Analysis software as significant function association of differentially expressed genes following introduction of miR-139-5p mimic. [score:3]
Therefore, miR-139-5p can act as a potential biomarker for early diagnosis and prognosis of ESCC and a therapeutic target for ESCC. [score:3]
Construction of miR-139-5p Overexpressed Cell Mo del. [score:3]
Differential Expression of miR-139-5p in ESCC Tissues and Adjacent Normal Tissues. [score:3]
To explore the actual association between NR5A2 and miR-139-5p, the relative expression of NR5A2 mRNA and miR-139-5p was determined in five ESCC cell lines. [score:3]
Identification of NR5A2 regulated by miR-139-5p and downstream genes. [score:2]
The deregulation of miR-139-5p was observed to be a frequent event in ESCC and other types of cancer [13], [22], [23]. [score:2]
miR-139-5p Regulates NR5A2 Protein and mRNA Level. [score:2]
D represents the relative expression levels of cyclin D1, cyclin E1, and MMP9 mRNA associated with cell cycle arrest and cell invasiveness in miR-139-5p mimic -transfected EC109 cells (red bar) compared with negative control cells (blue bar) using quantitative reverse transcription PCR. [score:2]
Considering that NR5A2 is regulated by miR-139-5p and showed no significant association with the risk for esophageal cancer, the results indicate that miR-139-5p is a more reliable indicator than NR5A2 for the early diagnosis of esophageal cancer. [score:2]
To identify the function of miR-139-5p in esophageal cancer oncogenesis, the above two total RNA samples were used for the genome-wide expression microarray assay. [score:2]
Further analysis of miR-139-5p association with clinicopathological features showed that miR-139-5p expression levels were significantly reduced in patients with lymph node metastasis compared with those without lymph node metastasis (P = 0.040, Table 2). [score:2]
Significant differences in miR-139-5p expression between cancer tissues and adjacent normal tissues were observed, and the average fold change decrease of miR-139-5p in cancer tissues was 14.065 compared with adjacent normal tissues. [score:2]
Cell cycle and apoptosis assay of miR-139-5p overexpression in EC109 cells. [score:2]
The present study confirmed a 14.065-fold decrease expression of miR-139-5p in ESCC tissues compared with normal tissues, which was significantly associated with an increased risk for esophageal cancer. [score:2]
Moreover, co-transfection of miR-139-5p mimics with wild-type 3′UTR constructs of NR5A2 showed a 2.7-fold decrease in NR5A2 expression compared with the mutant type of 3′UTR constructs of NR5A2. [score:2]
The results showed a cell cycle arrest in the G0/G1 phase upon treatment with miR-139-5p mimic, suggesting that miR-139-5p participates in the regulation of the G1/S phase transition during cell cycle progression. [score:2]
miR-139-5p Affects Cell Cycle and Invasiveness through Cyclin E1 and MMP9 Regulated by NR5A2. [score:2]
Relative expression of miR-139-5p and NR5A2 that were normalized against U6 and β-actin, respectively, were evaluated using Pearson correlation analysis. [score:1]
A 2 h pulse of EdU was found to label approximately one-third of the control cells, as expected for a rapidly dividing population (Figures 2A and 2C), but it only labeled approximately one-fourth of cells that were transfected with miR-139-5p mimic (Figures 2B and 2C). [score:1]
The protein levels of NR5A2 were determined in the EC109 cells transfected with miR-139-5p mimic or NC by Western blot analysis. [score:1]
The result showed a moderate negative correlation between miR-139-5p and NR5A2 (R = −0.398 for NR5A2 mRNA, and R = −0.370 for NR5A2 protein, respectively). [score:1]
To validate the mechanism of NR5A2 regulation by miR-139-5p, luciferase reporter assay was performed by transfecting the 3′UTR of NR5A2 constructs. [score:1]
G represents quantitation of migration following miR-139-5p transfection versus controls. [score:1]
EC109 cells were treated with miR-139-5p mimic (A) or negative control (B). [score:1]
As shown in Figure 5D, after normalization by β-actin, the mRNA levels of cyclin E1 and MMP9 were significantly changed in EC109 cells after transfection with the miR-139-5p mimic (P<0.05). [score:1]
0077068.g002 Figure 2 EC109 cells were treated with miR-139-5p mimic (A) or negative control (B). [score:1]
As shown in Figure 3A, for miR-139-5p transfected cells, the constituent ratio of cell cycle phases significantly differed from that in NC cells (x [2] = 45.70, P<0.0001). [score:1]
Flow cytometry was used to determine the effect of miR-139-5p on the cell cycle phase of EC109. [score:1]
After normalization by β-actin, the mRNA and protein levels of NR5A2 were significantly reduced in EC109 cells transfected with miR-139-5p mimic (P<0.05), as shown in Figures 5A and 5B. [score:1]
The effect of miR-139-5p on cell migratory activity was detected by cell scratch experiment. [score:1]
The effect of miR-139-5p on cell invasive capability was detected using a 24-well transwell plate (8 µm pore size, Corning, New York, USA). [score:1]
Associations of miR-139-5p expression with demographic and clinical characteristics. [score:1]
In this study, the tumor suppressive features of miR-139-5p were measured based on cell proliferation and cell cycle, migratory activity and invasion, and apoptosis. [score:1]
0077068.g003 Figure 3 (A) FACS analysis was performed to determine the constitution of cell cycle in miR-139-5p transfected cells and negative control cells. [score:1]
Odds ratios (OR) with 95% confidence intervals (95% CI) were calculated by conditional logistic regression to estimate the relative risk associated with miR-139-5p expression levels. [score:1]
The cell scratch experiment showed a significant difference between miR-139-5p treatment and NC at either the 24 h or 48 h time points after wounding (Figures 4A to 4G). [score:1]
EC109 cells (1×10 [6]) with miR-139-5p mimic or NC oligonucleotide were trypsinized and resuspended in 500 µL of binding buffer with 5 µL of Annexin V-FITC and 5 µL of propidium iodide. [score:1]
Figure 5C shows the luciferase signals from co-transfection of miR-139-5p mimics or NC with wild-type or mutant of 3′UTR constructs of NR5A2. [score:1]
Cell invasive ability of EC109 cells treated with miR-139-5p mimic (H) or negative control (I) was determined using a 24-well transwell plate. [score:1]
miR-139-5p Induces Late Apoptosis of ESCC Cells in vitro. [score:1]
NC and miR-21* are the negative and non-specific controls of miR-139-5p, respectively. [score:1]
Paired Student’s t-test was performed to evaluate the differences in miR-139-5p expression between tumor tissue group and adjacent normal tissue group. [score:1]
J represents the number of invading cells following miR-139-5p transfection versus controls. [score:1]
Briefly, EC109 cells (1×10 [4]) were seeded in each well of 96-well plates for transfection with miR-139-5p mimic or NC oligonucleotide. [score:1]
The figures show significantly reduction (P<0.01) in the proliferation rate in EC109 cells treated with miR-139-5p mimic. [score:1]
Briefly, EC109 cells (1×10 [6]) treated with miR-139-5p mimic or NC oligonucleotide were trypsinized and fixed in 70% ethanol at 4°C overnight. [score:1]
0077068.g004 Figure 4 A to F shows the effect of miR-139-5p transfection on cell migratory activity using cell scratch experiment. [score:1]
To assess the effect of miR-139-5p on cell migratory and invasive capability, cell scratch experiment and transwell invasive experiment were respectively conducted. [score:1]
A to F shows the effect of miR-139-5p transfection on cell migratory activity using cell scratch experiment. [score:1]
Briefly, 12 pmol of miR-139-5p mimic or NC was mixed with 2 µL of RNAiMAX reagent in 0.2 mL of OPTI-MEM (Invitrogen). [score:1]
Cells were transfected with either a miR-139-5p mimic or a scrambled NC (Guangzhou RiboBio Co. [score:1]
After normalization against β-actin, the mRNA levels of cyclin E1 and MMP9 were significantly reduced in EC109 cells transfected with the miR-139-5p mimic (P<0.05). [score:1]
C shows luciferase reporter assay for 3′UTR of NR5A2 regulated by miR-139-5p. [score:1]
Negative control (NC) and miR-21* represent the negative and non-specific control of miR-139-5p, respectively. [score:1]
The results imply that the alteration of miR-139-5p levels in ESCC cells may trigger major downstream events in carcinogenesis, which were classified by IPA. [score:1]
The results show that the mRNA and protein levels of NR5A2 were significantly reduced in EC109 cells when transfected with the miR-139-5p mimic. [score:1]
EC109 cells (5×10 [5]) were seeded in 6-well plates for transfection with miR-139-5p mimic or NC oligonucleotide. [score:1]
To investigate the potential functional roles of miR-139-5p in esophageal carcinogenesis, miR-139-5p expression was analyzed in five ESCC cell lines, and a miR-139-5p mimic treatment of an ESCC cell line was established for genome-wide microarray analysis. [score:1]
EC109 cells (1×10 [4]) treated with miR-139-5p mimic or NC were trypsinized and suspended in RPMI1640 medium supplemented with 10% FBS. [score:1]
Bar represents the luciferase signal ratio for Renilla over Firefly of miR-139-5p mimic or controls co-transfection with 3′UTR constructs of NR5A2 or control. [score:1]
Briefly, EC109 cells were seeded into a 96-well plate with a concentration of 10 thousand cells per well in a total volume of 100 µL and incubated for 24 h. Cells were then co -transfected with miR-139-5p mimic or controls and 3′UTR vector. [score:1]
The top interactional network of altered genes following the miR-139-5p mimic transfection. [score:1]
miR-139-5p can also induce the late apoptosis of ESCC cells in vitro and was further demonstrated to affect cell migratory activity and cell invasiveness. [score:1]
The apoptosis rate of EC109 cells transfected with miR-139-5p or NC using Annexin V-FITC and PI double staining was simultaneously determined. [score:1]
The cell percentage at different phases showed a cell cycle arrest in G0/G1 phase when treated with miR-139-5p mimic (P<0.05). [score:1]
[1 to 20 of 131 sentences]
2
[+] score: 252
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-200c, hsa-mir-200a, hsa-mir-328
In the present study, miR-139 was frequently suppressed in NSCLC, and overexpression of miR-139 suppressed invasion of lung cancer cells. [score:7]
As H3K27me3 was especially enriched in NCI-H2170 cells that had lowest expression of PDE2A and miR-139 (Fig. 2F), we tested whether DZNep, alone or in combination with histone deacetylation inhibitor TSA, can induce the expression of PDE2A and miR-139. [score:7]
In a systematic analysis of expression of 175 miRNAs using various human tissues, miR-139 was one of miRNAs whose expression showed the strongest correlation with expression of its host gene 20. [score:7]
As Miranda et al. reports that DZNep globally inhibits histone methylation and is not necessarily specific to EZH2 25, the effect of EZH2 knockdown on miR-139 and PDE2A expression was analyzed in two lung cancer cell lines. [score:6]
Suppression of miR-139 with its host gene PDE2A in primary NSCLCs and lung cancer cell linesIn primary NSCLCs, miR-139 expression was significantly suppressed compared with adjacent normal lung tissue (P < 1.0  × 10 [−11], Fig. 1A). [score:6]
This is the first report on the tumor suppressive function of this miRNA in lung cancer, and our results confirms that the downregulation of miR-139 plays an important role in metastatic process of various types of human cancer. [score:6]
Expression of a long PDE2A transcript was detected in the brain, but not in the 25 lung cancer cell lines and NHBE cells even after 40 real-time PCR amplification cycles, suggesting that miR-139 is cosuppressed with the short PDE2A transcript in lung cancer cells. [score:5]
Ectopic expression of miR-139 in lung cancer cell lines suppressed the invasion through the extracellular matrix. [score:5]
We first noticed that patients with distant lymph node metastasis (N2 disease) had lower expression of miR-139 (Student's t-test P = 0.01) and we determined the cut-off value that best discriminate patients with distant lymph node metastasis from other patients. [score:5]
Our results also confirmed that miR-139 expression was correlated with expression of its host gene in lung cancer cell lines and primary NSCLCs. [score:5]
As shown in Figure 3A and B, DZNep alone did not largely affect the expression of PDE2A and miR-139, but the combination of DZNep and TSA significantly induced miR-139 expression together with its host gene PDE2A. [score:5]
DZNep, 3-Deazaneplanocin A; TSA, Tricostatin A. Induction of miR-139 by the combination of TSA and EZH2 knockdownAs EZH2 has histone methyltransferase activity with substrate specificity for H3K27 22, the effect of EZH2 knockdown on miR-139 and PDE2A expression was analyzed in lung cancer cells. [score:5]
Overexpression of miR-139 using a U6 promoter -based expression vector 5, 19 did not affect the proliferation (Fig. 5B) nor the transwell cell migration (Fig. 5C). [score:5]
We have also found that pharmacologic inhibition of both EZH2 and histone deacethylase (HDAC) induced PDE2A and miR-139 expression, which is consistent with the report that EZH2 require HDAC for its gene silencing activity 24. [score:5]
Ectopic expression of miR-139 suppresses the proliferation, migration, and invasion of esophageal and colorectal cancer 14, 15. [score:5]
Figure 5Overexpression of miR-139 in NCI-H2170 and ABC-1. (A and E) Stable overexpression of miR-139 in NCI-H2170 and ABC-1 cells. [score:5]
The expression of miR-139 was significantly associated with the expression of PDE2A (Fig. 1B). [score:5]
The expression of PDE2A was also induced by TSA and EZH2 knockdown, although the degree of induction was smaller than that of miR-139 (Fig. 4E and F). [score:4]
These studies suggest that the downregulation of miR-139 is a common feature of wide spectrum of human malignancies. [score:4]
In contrast, miR-139 expression was independent of tumor size or EGFR mutation (Table 1B). [score:4]
Figure 4Effect of EZH2 knockdown on miR-139 and PDE2A expression. [score:4]
In primary NSCLCs, miR-139 expression was significantly suppressed compared with adjacent normal lung tissue (P < 1.0  × 10 [−11], Fig. 1A). [score:4]
These results suggested that the loss of miR-139 expression (which was independent of oncogenic driver mutation) was associated not with the size of the primary tumor but with the metastatic and invasive features of lung cancer. [score:4]
DZNep, 3-Deazaneplanocin A; TSA, Tricostatin A. As EZH2 has histone methyltransferase activity with substrate specificity for H3K27 22, the effect of EZH2 knockdown on miR-139 and PDE2A expression was analyzed in lung cancer cells. [score:4]
The combination of TSA and EZH2 knockdown also induced PDE2A expression, but the degree of induction was smaller than that observed in miR-139. [score:4]
Downregulation of miR-139 has also been shown to play an important role in the HER2 -mediated metastatic process of gastric cancer 13. [score:4]
In the present study, miR-139 was frequently suppressed in lung cancer cell lines and primary NSCLCs. [score:3]
Expression of miR-139 and PDE2A in 25 lung cancer cell lines and NHBE. [score:3]
Increased H3K27me3 and decreased H3K4me3 in lung cancer cell lines with low miR-139 and PDE2A expressionAccording to the UCSC Genome Bioinformatics Site (http://genome. [score:3]
Our results suggest that miR-139 plays an important role in lung cancer metastasis not only in the very early stage of carcinogenesis, but also in the advanced stage of disease progression. [score:3]
These findings indicate that miR-139 is suppressed with its host gene PDE2A in NSCLC. [score:3]
In a univariate analysis (chi-square test), low expression of miR-139 was significantly associated with distant lymph node metastasis (P = 0.038, Table 1B). [score:3]
As intronic miRNAs are sometimes expressed with their host genes in a coordinated manner 20, we measured the expression of miR-139 and PDE2A in 25 lung cancer cell lines and NHBE cells (Fig. 1B). [score:3]
We divided the patients into two groups based on the miR-139 expression using this cut-off value. [score:3]
To evaluate the function of miR-139 in NSCLC, we overexpressed miR-139 in NCI-H2170 cells that has lowest miR-139 expression (Fig. 5A). [score:3]
The vertical axis indicates miR-139 expression relative to the control vector. [score:3]
Suppression of invasion by miR-139 in lung cancer cells. [score:3]
Increased H3K27me3 and decreased H3K4me3 in lung cancer cell lines with low miR-139 and PDE2A expression. [score:3]
The association between miR-139 expression and distant lymph node metastasis or histological invasiveness was confirmed further using a multivariate analysis (stepwise logistic regression analysis). [score:3]
In conclusion, H3K27me3 -mediated silencing of miR-139 may have an important role in lung cancer metastasis, and miR-139 expression is a promising biomarker of an invasive and metastatic phenotype of lung cancer. [score:3]
The explanatory variables used were age, gender, smoking, histology, tumor size, and miR-139 expression. [score:3]
In addition, miR-139 expression (P = 0.016, OR = 5.415) and smoking (P = 0.028, OR = 4.749) were associated with the presence of both lymphatic and venous invasion, whereas other clinical variables (age, gender, histology, and tumor size) were not associated with the presence of both lymphatic and venous invasion (Table 1D). [score:3]
However, miR-139 significantly suppressed the cell invasion through the extracellular matrix (Fig. 5D). [score:3]
Moreover, low expression of miR-139 was significantly associated with the presence of both lymphatic and venous invasion (P = 0.022, Table 1B). [score:3]
A mild but significant correlation was observed between miR-139 and PDE2A expression in primary NSCLCs and adjacent normal lung tissues (Fig. 1C). [score:3]
Induction of miR-139 with its host gene PDE2A by the combination of DZNep and TSAIt is reported that DZNep inhibits H3K27me3 in cancer cells 21. [score:3]
In a multivariate analysis, miR-139 expression (P = 0.035, odds ratio [OR] = 3.993) and tumor size (P = 0.003, OR = 6.629) were associated with distant lymph node metastasis, whereas other clinical variables (age, gender, smoking status, and histology) were not associated with distant lymph node metastasis (Table 1C). [score:3]
Interestingly, miR-139 expression was preferentially lost in the final step of carcinogenesis: from in situ carcinoma to invasive squamous cell carcinoma. [score:3]
To further analyze the transcriptional regulation of the short PDE2A transcript, we performed ChIP assay of NHBE cells and five lung cancer cell lines with various levels of PDE2A and miR-139 expression (Fig. 2B and C). [score:3]
These observations showed that the loss of miR-139 expression was significantly associated with the invasive and metastatic phenotype of primary NSCLCs. [score:3]
Figure 1Expression of miR-139 in lung cancer. [score:3]
Suppression of miR-139 with its host gene PDE2A in primary NSCLCs and lung cancer cell lines. [score:3]
Association between miR-139 expression and invasive and metastatic phenotype in primary NSCLCs. [score:3]
This difference may be explained by the activation of a novel miR-139 promoter that is different from its host gene, or the secondary effect such as the induction of miRNAs that target PDE2A. [score:3]
In primary NSCLCs, decreased expression of miR-139 was significantly associated with distant lymph node metastasis and histological invasiveness. [score:3]
Neither significant loss in copy number nor mutations were detected at the miR-139 locus. [score:2]
The combination of TSA and EZH2 knockdown led to robust induction of miR-139, which confirms that H3K27me3 is involved in the silencing of miR-139 in lung cancer. [score:2]
Further research will fully elucidate the regulation of miR-139 in NSCLC. [score:2]
We think it would be interesting to study whether knockdown of miR-139 enhances invasive phenotype of lung cancer cells. [score:2]
The purpose of the present study was to analyze the function and mechanism of transcriptional regulation of miR-139 in NSCLC. [score:2]
Induction of miR-139 by the combination of TSA and EZH2 knockdown. [score:2]
MiR-139 reportedly target Rho-kinase 2 in hepatocellular carcinoma 11, NR5A2 in esophageal cancer 14, NOTCH1 and IGF1R in colorectal cancer 15, 28. [score:2]
The combination of TSA and EZH2 knockdown induced robust induction of miR-139 in NCI-H2170 and ABC-1 cells (Fig. 4C and D). [score:2]
The PCR products of the miR-139 locus were sequenced to analyze the mutation status of miR-139. [score:2]
Our results show that H3K27me3 plays a role in the regulation of miR-139 and PDE2A but other histone modifications may also be involved. [score:2]
These results suggest that miR-139 is coregulated with PDE2A at least in lung cancer cells. [score:2]
Induction of miR-139 with its host gene PDE2A by the combination of DZNep and TSA. [score:1]
MiR-139 has been recently reported to function as an antimetastatic miRNA in hepatocellular carcinoma 11 and breast cancer 12. [score:1]
We found that miR-139 was epigenetically silenced with its host gene PDE2A by H3K27me3 in lung cancer cells. [score:1]
Figure 3Induction of miR-139 and PDE2A by DZNep and TSA. [score:1]
A Pearson's correlation coefficient was calculated between miR-139 and PDE2A expression. [score:1]
Alterations in the copy number of the miR-139 locus were determined using real-time PCR -based method 18. [score:1]
The chromatin immunoprecipitation (ChIP) assay was performed to analyze the transcriptional regulation of miR-139. [score:1]
Recently, miR-139-5p (denoted thereafter as miR-139) has been shown to function as an antimetastatic miRNA in hepatocellular carcinoma 11 and breast cancer 12. [score:1]
Further investigation is required to elucidate the molecular mechanism which links miR-139 expression and an aggressive phenotype of lung cancer. [score:1]
We showed here that the miR-139 was silenced with its host gene PDE2A by H3K27me3. [score:1]
Collectively, these findings suggested that miR-139 was epigenetically silenced with its host gene PDE2A by histone methylation and this process was independent of DNA methylation. [score:1]
These results show that miR-139 has anti-invasive function in lung cancer cells. [score:1]
Finally, we analyzed the changes in copy number of the miR-139 locus to exclude the possibility of deletion of this chromosomal region (Fig. S1C). [score:1]
[1 to 20 of 79 sentences]
3
[+] score: 196
We also revealed that the expression of miR-139-5p was upregulated in liver metastatic tissues compared to matching primary tissues, and illustrated in a mouse mo del that an overexpression of miR-139-5p in a CRC cell line resulted in higher peritoneal metastasis than the respective control cell line. [score:7]
MiR139-5p regulates EMT-related genes in vitroIn order to confirm that miR-139-5p, a noncoding RNA, regulates EMT-related genes (ZEB1, ZEB2, E-cadherin), we overexpressed miR-139-5p by transiently transfecting CRC cell lines with miR-139-5p mimics or scrambled controls, and evaluated the protein expression of these downstream target genes. [score:7]
Western blot analysis showed that overexpression of miR-139-5p in CRC cell lines resulted in reduced ZEB1 and ZEB2 protein expression, while E-cadherin was upregulated compared to negative control transfected cells (Fig. 4E). [score:7]
In pancreatic cancer and ovarian granulosa cell tumor the expression of miR-139-5p was found to be upregulated, indicating its potential role as an oncogene 39 40. [score:6]
It was reported that miR-139-5p was downregulated in hepatocellular carcinoma 19, parathyroid carcinoma 43, and gastric cancer 44 with in vitro data suggesting that the inhibition of miR-139-5p results in increased proliferation 45. [score:6]
In order to confirm that miR-139-5p, a noncoding RNA, regulates EMT-related genes (ZEB1, ZEB2, E-cadherin), we overexpressed miR-139-5p by transiently transfecting CRC cell lines with miR-139-5p mimics or scrambled controls, and evaluated the protein expression of these downstream target genes. [score:6]
First, we assessed the expression of miR-139-5p in several CRC cell lines and selected two CRC cell lines with lowest miR-139-5p expression, R KO and Caco-2 (Supplemental Fig. 3). [score:5]
Furthermore, the expression of ZEB1 and ZEB2 inversely correlated with miR-139-5p expression (r = −0.36, P < 0.05 and r = −0.401, P < 0.05 respectively; Fig. 4B,C), while E-cadherin showed a positive association with miR-139-5p (r = 0.41, P < 0.05; Fig. 4D). [score:5]
Moreover, we showed that the expression of miR-139-5p is upregulated in metastatic tissues compared to matching primary tissues and it is inversely correlated with EMT -associated genes. [score:5]
The present study showed that miR-139-5p functions similarly to miR-200c, i. e. both miRNAs are upregulated in primary tumors and in serum of patients who undergo tumor relapse. [score:4]
To determine whether miR-139-5p is upregulated in the primary cancers of patients who had recurrence within three years of their cancer, we evaluated the expression of miR-139-5p in two independent clinical cohorts. [score:4]
The dysregulation of miR-139-5p expression has been reported to occur in a number of cancers. [score:4]
Moreover, the expression of miR139-5p in peripheral blood was significantly higher in prostate cancer patients compared to patients with benign prostatic hyperplasia and healthy controls, and much higher expression of peripheral blood miR-139-5p was detected in prostate cancer patients with more advanced stage and more aggressive tumors 42. [score:4]
Furthermore, we showed consistent upregulation of miR-139-5p in the serum samples of CRC patients with recurrence. [score:4]
To confirm whether CRC cells with high levels of miR-139-5p are more likely to attach themselves to the metastasis sites compared to those cells with lower expression of this miRNA, we overexpressed miR-139-5p CRC cell lines and used these cells in a mouse mo del of peritoneal metastasis. [score:4]
Collectively, these data indicate that miR-139-5p is involved in EMT and upregulation of circulating miR-139-5p may promote colonization of cancer cells and initiate metastasis. [score:4]
Interestingly, ZEB1 and ZEB2, two transcription factors involved in this process, are downstream targets of miR-139-5p 23. [score:3]
The expression levels of miR-139-5p and EMT-related genes (ZEB1, ZEB2, and E-cadherin) with primary CRC tissue vs. [score:3]
The multivariate analysis adjusted for these parameters validated that high miR-139-5p expression was confirmed to be one of independent biomarkers for predicting early recurrence in CRC patients (HR = 2.30, 95% CI = 1.19–4.46 P = 0.01; Table 1). [score:3]
ROC curves were established to discriminate the patients with or without recurrence, and the Youden’s index was used to determine the optimal cutoff thresholds for miR-139-5p expression to predict the recurrence. [score:3]
Intriguingly, miR-139-5p was significantly upregulated in metastatic CRCs in the liver compared to primary CRCs (P = 0.0006; Fig. 4A). [score:3]
Consistent with the results we obtained from the TCGA dataset used in our discovery phase, the patients with higher levels of miR-139-5p had significantly poorer RFS than those with lower expression of this miRNA in both cohorts (P = 0.005 and P = 0.003; log-rank test respectively; Fig. 3A,B). [score:3]
In contrast, there are few reports in various cancers that miR-139-5p may also act as a tumor suppressor. [score:3]
The current study demonstrated that miR-139-5p was upregulated in primary cancer tissues of patients with recurrence compared to those who did not. [score:3]
Lastly, in an in vivo animal mo del we demonstrated that overexpression of miR-139-5p resulted in enhanced peritoneal metastasis. [score:3]
Therefore, we suspect that despite the fact that miR-139-5p may act as a tumor suppressor in early-stage cancers, it may play a significant role in initiation of metastasis in CRC. [score:3]
The subsequent multivariate analysis confirmed these results and showed high miR-139-5p expression was one of independent markers for predicting early recurrence in CRC patients (HR = 2.63, 95% CI = 1.13–6.11 P = 0.02; Table 1). [score:3]
Overexpression of miR-139-5p induces peritoneal metastasis. [score:3]
Mechanistically, miR-139-5p and miR-200c share the same EMT -associated downstream target genes such as ZEB1 and ZEB2, a possible explanation for their functional similarities. [score:3]
Furthermore, we have also demonstrated that the expression of miR-139-5p in serum, not just tissue, appears to serve as a possible marker for CRC recurrence. [score:3]
As expected, the patients with higher serum levels of miR-139-5p had a significantly shorter RFS than those with lower expression of this miRNA (P = 0.004; log-rank test; Fig. 3E). [score:3]
MiR-139-5p is upregulated in the primary tumors with recurrent CRC. [score:3]
In Cohort 1, the expression of miR-139-5p in primary CRC tissues in patients who recurred within 3 years of surgery was significantly higher than in CRC tissues from patients who did not recur (P < 0.05; Fig. 3A). [score:3]
Moreover, we assessed whether miR-139-5p expression was influenced by microsatellite instability (MSI) status in the TCGA dataset of 105 stage III CRC patients. [score:3]
Moreover, we used the Cox proportional hazard regression mo del to determine whether miR-139-5p expression was an independent risk factor for RFS (Table 1). [score:3]
In addition, we assessed whether there were differences in miR-139-5p expression based on the metastasis sites in Cohort 1 patients. [score:3]
An AUC value of 0.75 for serum miR-139-5p indicated that the expression of this miRNA could distinguish CRC patients with versus those without tumor recurrence (95% CI = 0.59–0.87 P = 0.001, sensitivity = 64% specificity = 80%; Fig. 3E). [score:3]
The assessment of the internal cavity of mice showed that miR-139-5p -overexpressing cells had a significantly greater number of disseminated nodules than cells transfected with the scrambled control (P < 0.05; Fig. 5B). [score:3]
Collectively, our results showed that miR-139-5p expression in tissue, as well as in serum, is a potential of recurrence I CRC patients. [score:3]
While these outcomes are in conflict with the results of the previous studies, there are several miRNAs that appear to behave similarly to miR-139-5p, acting as both oncogenes and tumor suppressors in different types of human cancers. [score:3]
A similar finding was observed in Cohort 2; miR-139-5p expression was significantly higher in tumors from CRC patients who recurred within three years compared to those who did not experience tumor relapse (P < 0.05; Fig. 3B). [score:2]
Serum miR-139-5p expression was significantly elevated in stage I-III CRC patients who recurred compared to those who did not recur (15 with recurrence versus 26 without recurrence; P = 0.002; Fig. 3C). [score:2]
MiR-139-5p expression levels via qRT-PCR with vs. [score:2]
When compared between liver (n = 11), lung (n = 12) and other metastasis sites (n = 8), there were no statistical differences observed in miR-139-5p expression (Supplemental Fig. 1). [score:2]
MiR-139-5p expression levels via qRT-PCR with recurrence vs. [score:2]
Mir-139-5p expression levels in two independent tissue validation cohorts and a serum validation cohort. [score:2]
MiR-139-5p Overexpression. [score:2]
MiR-139-5p is upregulated in liver metastatic CRC compared to primary CRCs. [score:2]
Next, in order to evaluate our hypothesis that miR-139-5p is involved in the metastatic process in CRC, we analyzed the expression levels of miR-139-5p in 30 pairs of primary CRC and their matching metastatic liver tumors. [score:1]
Furthermore, serum miR-139-5p levels in stage III and stage IV CRC patients were higher than those in stage I CRC patients (P = 0.04 and P = 0.003 respectively; Fig. 3D). [score:1]
without recurrence within 3 years after surgery, and RFS analysis of miR-139-5p. [score:1]
In conclusion, for the first time, we have identified miR-139-5p as a potential novel biomarker for tumor recurrence in CRC patients. [score:1]
In addition to this discovery step, we analyzed two independent patient cohorts to validate that miR-139-5p is a potential biomarker for CRC recurrence. [score:1]
Furthermore, no mice in the control group developed any tumors (Fig. 5C), indicating that miR-139-5p enhances metastatic potential of CRC cells. [score:1]
Collectively, the results from these experiments showed that miR-139-5p is a promising biomarker for CRC recurrence. [score:1]
In order to truly test the biomarker potential of circulating miR-139-5p, a prospectively collected longitudinal study is required. [score:1]
We then validated the biomarker potential of miR-139-5p to serve as a recurrence prediction biomarker in two independent clinical cohorts. [score:1]
Immune deficient mice were injected intraperitoneally with 3 × 10 [6] cells transfected with either miR-139-5p mimic or scrambled control (n = 11 each group) and all mice were sacrificed 60 days post-injection. [score:1]
Therefore, we have begun a prospective collection of patient samples, both tissue and serum, and plan to assess the efficacy of miR-139-5p as a potential monitoring marker for CRC recurrence. [score:1]
Next, we assessed whether the circulating levels of miR-139-5p levels in the serum of CRC patients are predictive of relapse in Cohort 3 (Supplemental Table 5). [score:1]
Furthermore, we showed that circulating miR-139-5p was able to discriminate patients who were going to recur within three years from those patients who did not undergo relapse during this time span. [score:1]
Univariate analysis of Cohort 1 revealed that high levels of miR-139-5p (P < 0.001), higher pathological T stage (T3/4; P = 0.01) and lymph node metastasis (P = 0.001) were significantly associated with poor RFS. [score:1]
We demonstrated that miR-139-5p was significantly higher in tumors from recurrent versus non-recurrent CRC patients (Fig. 2B), while no significant differences were observed in the levels of let-7e, miR-181a, or miR-181b in CRCs from patients who relapsed versus those who did not. [score:1]
While in these previous studies the rationale for candidate miRNA selection was primarily based on their putative functions, in this study, we identified miR-139-5p as a CRC recurrence prediction biomarker using a systematic and comprehensive miRNA discovery strategy. [score:1]
Serum miR139-5p is a tumor recurrence predictive biomarker in CRC. [score:1]
MiR139-5p regulates EMT-related genes in vitro. [score:1]
Based upon these observations, we selected miR-139-5p for further testing as a candidate miRNA to serve as a biomarker for CRC recurrence. [score:1]
Of the five candidate miRNAs analyzed, four miRNAs (let-7e, miR-139-5p, miR-181a, miR-181b) were able to differentiate those with vs. [score:1]
Likewise, in Cohort 2, the univariate analysis revealed high miR-139-5p (P = 0.002), high pathological T stage (T3/4; P = 0.01) and lymph node metastasis (P = 0.02) were significantly associated with poor RFS. [score:1]
Next, in order to evaluate whether miR-139-5p expression can predict CRC recurrence, we assessed the RFS using Kaplan-Meier analysis. [score:1]
In addition, serum levels of miR-139 were shown to be significantly increased in adrenocortical cancer 41. [score:1]
To establish a mouse peritoneal metastasis mo del, 3 × 10 [6] Caco-2 cells transfected with miR-139-5p mimic or the negative control were injected intraperitoneally into mice. [score:1]
non-recurrence within 3 years after surgery, and RFS analysis of miR-139-5p. [score:1]
ROC curve analysis was also used to evaluate whether serum miR-139-5p expression levels could distinguish patients with or without CRC recurrence. [score:1]
[1 to 20 of 74 sentences]
4
[+] score: 190
Yonemori et al. found that the expression of miR-139-5p/miR-139-3p in bladder cancer tissue is downregulated compared to normal bladder epithelia and overexpression of miR-139-5p/miR-139-3p in bladder cells significantly inhibited cell migration and invasion by targeting MMP11 [25]. [score:11]
HOXA10 expression was downregulated in endometrial cancer cells after miR-139-5p overexpression. [score:8]
These findings indicate that miR-139-5p targets the HOXA10 transcript and suppresses endometrial cancer cell growth and migration, suggesting that miR-139-5p acts as a tumor suppressive role in human endometrial cancer pathogenesis. [score:7]
Similarly, overexpression of miR-139-5p also inhibits epithelial–mesenchymal transition, migration and invasion of hepatocellular carcinoma cells by targeting ZEB1 and ZEB2 [15]. [score:7]
Downregulation of miR-139-5p expression occurs in EC tissues. [score:6]
We predicted that miR-139-5p, is a regulator of HOXA10 expression, based on PicTar, TargetScan, and miRBase database. [score:6]
This study indicates the levels of miR-139-5p in EC tissues were markedly reduced compared to normal endometrium tissues and overexpression of miR-139-5p in endometrial cancer cells markedly reduced cell viability and migration, and suppressed HOXA10 expression. [score:6]
Consistent with other types of cancer, transient introduction of miR-139-5p inhibiting cell proliferation, metastasis, and promoting apoptosis by targeting oncogenic c-Met in lung cancer cell line A549 and SK-MES-1 [16]. [score:5]
Furthermore, miR-139-5p expression was significantly downregulated in endometrial cancer tissues as compared to matched normal tissues by RT-PCR (Fig.   1b). [score:5]
The expression level of HOXA10 was significantly increased in endometrial cancer tissues, which was inversely correlated with miR-139-5p expression in clinical endometrial cancer tissues. [score:5]
The 3’-UTR of HOXA10 cDNA which contains a putative target region for miR-139-5p (bold stands for the putative target site for miR-139-5p). [score:5]
The 3ʹ-untranslated regions (3ʹ-UTRs) of human HOXA10 cDNA with the putative target sites for miR-139-5p (sequences were provided in 1) were synthesized and then inserted at the XbaI site downstream of the luciferase gene in the pGL3-control (Promega) vector by Integrated Biotech Solutions Co. [score:5]
Overexpressed miR-139-5p significantly inhibited endometrial cancer cell viability and migration. [score:5]
In confirmation of this functional interaction, overexpression of miR-139-5p reduced HOXA10 protein expression in EC cell lines. [score:5]
MiR-139-5p expression was significantly down-regulated in EC tissues compared to that in normal tissues (Fig.   1a). [score:4]
Next, we performed Western blotting to confirm downregulation of HOXA10 protein following transfection of miR-139-5p in Ishikawa and ECC1 EC cells. [score:4]
Here, we found that miR-139-5p acts as a tumor-suppressor gene involved in EC development. [score:4]
In this study, target prediction software identified a miR-139-5p binding site in the 3′-UTR of HOXA10, and dual-luciferase reporter assays confirmed that HOXA10 is target of miR-139-5p. [score:4]
To determine the role of miR-139-5p in endometrial cancer development, we examined the expression of miR-139-5p in twenty-five endometrial cancer samples and fifteen adjacent normal tissues by RT-PCR. [score:4]
Downregulation of miR-139-5p is also detected in esophageal squamous cell carcinoma (ESCC). [score:4]
Furthermore, we explored whether HOXA10 is the target gene of the miR-139-5p. [score:3]
We demonstrated that miR-139-5p was down-regulated in human endometrial cancer compared to their matched adjacent non-tumor tissues. [score:3]
Overexpression of miR-139-5p reduced ESCC cell proliferation, migration and invasion [14]. [score:3]
Graphical presentation in b. c A plot of the relative expression of miR-139-5p vs HOXA10 showed an inverse correlation between the two items. [score:3]
Fig.  2HOXA10 is a candidate target of miR-139-5p. [score:3]
Our results suggest that miR-139-5p has as a tumor suppressive role in human EC pathogenesis. [score:3]
Significantly lower expression of miR-139-5p was detected in EC tissues than that in adjacent normal tissues. [score:3]
HOXA10 is a target gene of miR-139-5p. [score:3]
a The expression level of miR-139-5p in EC tissues (n = 25) and adjacent normal tissues (n = 15). [score:3]
Using these programs, we selected HOXA10 as a miR-139-5p target gene for further study, as HOXA10 was important for malignant behavior in other types of cancer (Fig.   2a). [score:3]
The protein expression levels of HOXA10 were significantly repressed in miR-139-5p -transfected cells in comparison with miR-control transfected cells (Fig.   2c, d). [score:3]
c, d I HOXA10 expression levels, by western blot analysis, in ECC1 and Ishikawa cells upon miR-139-5p or negative control reintroduction. [score:3]
In HEK-293T cells, a significant decrease in relative luciferase activity was noted when pGL3-HOXA10-3′-UTR was co -transfected with the miR-139-5p mimic but not with the miRNA mimic control, suggesting that HOXA10 is the target gene of the miR-139-5p (Fig.   2b). [score:3]
We constructed a luciferase reporter vector with the putative HOXA10 3′-UTR target site for the miR-139-5p downstream of the luciferase gene (pGL3-HOXA10-3′-UTR). [score:3]
a Computational analysis identified that HOXA10 may be a potential target of miR-139-5p, and the predicted binding sequences of HOXA10 3′-UTR and miR-139-5p were marked. [score:3]
The relative expression of miR-139-5p was normalized to U6, and calculated using the 2 [−ΔΔCt] method (ΔCt = Ct [target gene] − Ct [internal control]) [23]. [score:3]
Our findings suggest that miR-139-5p may act as a tumor suppressor in endometrial cancer and miR-139-5p may be a potential therapeutic agent for endometrial cancer. [score:3]
b Dual luciferase assay performed in HEK-293T cells confirms that HOXA10 is the target gene of the miR-139-5p. [score:2]
Luciferase reporter assay and western blot were used to confirm targeting of HOXA10 by miR-139-5p. [score:2]
MiR-139-5p suppresses the viability and migration of the Ishikawa and ECC1 endometrial cancer cell lines. [score:2]
In their study on intestinal inflammation and colorectal cancer, Zou et al. found that miR-139-5p knockout mice are highly susceptible to colitis and colon cancer, accompanied by elevated proliferation and decreased apoptosis, as well as an increased production of inflammatory cytokines, chemokines and tumorigenic factors [17]. [score:2]
Computational algorithm in combination with dual luciferase reporter assays identified HOXA10 as the target of miR-139-5p. [score:2]
However, the role of miR-139-5p in EC development, especially regarding its link with HOXA10, has not been explored yet. [score:2]
This study aimed to investigate the miR-139-5p expression and to analyze its function and underlying molecular mechanism in endometrial cancer. [score:1]
Ishikawa and ECC1 cells transfected with miR-139-5p mimics or mimics control were seeded in 6-well plates. [score:1]
was used to study the effect of miR-139-5p on EC cell migration. [score:1]
The number of migrated cells of EC cells with miR-139-5p were decrease much more than the mimics NC group. [score:1]
Luciferase reporter vector together with the miR-139-5p mimic or the miRNA mimic control were transfected into HEK-293T cells. [score:1]
In the tumor -associated miRNAs, the mechanism of miR-139-5p in cancer initiation and progression drew our attention, because miR-139-5p has been found to perform various biological functions in other types of malignancy, such as bladder, colon, esophageal, liver and lung cancer [14– 17]. [score:1]
An inverse correlation (R [2] = 0.9126, P < 0.01) was observed between miR-139-5p and HOXA10 using Spearman’s correlation analysis (Fig.   3c). [score:1]
In the present study, we investigated the expression of miR-139-5p in human EC and paired adjacent normal tissues, and explored the effects of miR-139-5p on cell growth and migration in vitro. [score:1]
miR-139-5p HOXA10 Endometrial cancer Viability Migration Endometrial cancer (EC) is the most frequent gynecological cancer and the fourth most common cancer for women in the developed world [1]. [score:1]
Several study’s show that miR-139-5p is involved in the tumorigenesis and metastasis of various cancers. [score:1]
was carried out using the protocol described previously and briefly [24], cells were transfected with NC, miR-139-5p, as described above. [score:1]
After Ishikawa and ECC1 cells were transfected with the miR-139-5p mimics or mimics control, the was used to determine the relative cell growth activity at 1 h post-transfection. [score:1]
In lung cancer, sun et al. showed that the level of miR-139-5p is significantly reduced in human lung cancer tissues and the low level of miR-139-5p correlates with survival of lung cancer patients [16]. [score:1]
Expression of miR-139-5p was measured using qRT-PCR. [score:1]
Then, two hundred ng of pGL3-HOXA10-3ʹ-UTR plus eighty ng of pRL-TK (Promega) were co -transfected with 60 pmol of miR-139-5p mimic or mimic control using Lipofectamine 2000 (Invitrogen) following the manufacturer’s protocol. [score:1]
miR-139-5p mimics were synthesized by GenePharma (Shanghai, People’s Republic of China). [score:1]
A significant decrease in relative luciferase activity was noted when pGL3-HOXA10-3′-UTR was co -transfected with the miR-139-5p mimic but not with the miRNA mimic control. [score:1]
[1 to 20 of 60 sentences]
5
[+] score: 138
XIST expression was upregulated by miR-139 inhibitor, whereas downregulated by ectopic miR-139 expression (Figure 5C). [score:13]
Further, miR-139 expression was downregulated, whereas β-catenin expression was upregulated in PF tissues. [score:11]
Results showed that in IMR-90 cells, the luciferase activity of wt-XIST vectors was significantly suppressed by miR-139 mimics, promoted by miR-139 inhibitor; after mutation on the putative binding site of miR-139 in XIST, the effect of miR-139 mimics or miR-139 inhibitor on luciferase activity was abolished (Figure 4B). [score:8]
After sh-XIST -induced XIST knockdown, miR-139 expression was upregulated (Figure 5A). [score:7]
Results showed that in PF tissues, miR-139 was downregulated, whereas β-catenin was upregulated (Figure 6A and 6B). [score:7]
Similarly, the luciferase activity of wt-β-catenin was promoted by miR-139 inhibitor; the effect of miR-139 inhibitor was abolished after mutation on the putative binding site (Figure 4C). [score:6]
In the present study, we demonstrated that XIST inversely regulated miR-139 expression by directly binding; in addition, β-catenin, an essential factor in Wnt/β-catenin signaling which has been reported to play a promotive role in PF [25– 27], could directly bind to miR-139 on an almost identical binding site. [score:6]
Moreover, when co -transfected with sh-XIST and wt-β-catenin/mut-β-catenin, similar results as co-transfecting miR-139 mimics and wt-β-catenin/mut-β-catenin were observed: luciferase activity of wt vector was suppressed by sh-XIST; sh-XIST -induced suppression of luciferase activity was abolished by mutation on binding site (Figure 4D), suggesting sh-XIST exerts similar function as miR-139 mimics. [score:6]
miR-139 mimics or miR-139 inhibitor was transfected into MLFCs to achieve ectopic miR-139 expression or miR-139 inhibition, as verified by using real-time PCR assay (Figure 5B). [score:6]
The protein levels of β-catenin were significantly increased by miR-139 inhibitor (total, nucleus and cytoplasm), reduced by sh-XIST (total, nucleus and cytoplasm); the promotive effect of miR-139 inhibitor on β-catenin protein could be partially reversed by sh-XIST (total, nucleus and cytoplasm) (Figure 5D and 5E). [score:5]
Similar as β-catenin, the protein levels of Collagen I and α-SMA were increased by miR-139 inhibitor, reduced by sh-XIST; the promotive effect of miR-139 inhibitor on Collagen I and α-SMA protein levels could be partially reversed by sh-XIST (Figure 5F). [score:5]
In response to XIST knockdown, β-catenin in nucleus and cytoplasm, Collagen I and α-SMA protein levels were reduced; in response to miR-139 inhibition, the indicated protein levels were increased. [score:4]
Moreover, miR-139 inhibition partially reversed the effect of XIST knockdown on the indicated protein levels. [score:4]
Figure 5(A) miR-139 expression in response to XIST knockdown in MLFCs was determined by using real-time PCR. [score:4]
Through Wnt/β-catenin signaling, XIST/miR-139 regulates ECM protein expression in MLFCs. [score:4]
A wt-XIST luciferase reporter gene vector (human or mice), a mut-XIST vector containing a 7 bp (human) or a 6 bp (mice) mutation on putative binding site of miR-139, a wt-β-catenin vector (human or mice), a mut-β-catenin vector containing a 5 bp mutation on putative binding site of miR-139 (human or mice) was constructed. [score:3]
After co-introducing sh-XIST and miR-139 inhibitor into MLFCs, β-catenin, Collagen I and α-SMA protein levels were monitored. [score:3]
Expression of miR-139 and β-catenin and their correlations with XIST in tissues. [score:3]
A wt-XIST luciferase reporter gene vector, a mut-XIST vector containing a 7 bp (human) or 6 bp (mice) mutation on putative binding site of miR-139, a wt-β-catenin vector, a mut-β-catenin vector containing a 5 bp mutation on putative binding site of miR-139 was constructed (Figure 4A and 4F). [score:3]
Moreover, miR-139 expression was inversely correlated with XIST and β-catenin, respectively; XIST and β-catenin was positively correlated, further indicating the positive role of XIST in PF, and that XIST competes with β-catenin for miR-139 binding to promote PF progression. [score:3]
After cultured overnight, cells were co -transfected with the wild-type and mutated XIST or wild-type and mutated β-catenin 3′UTR reporter plasmid or pRL-TK plasmids and miR-139 mimics or miR-139 inhibitor. [score:3]
Next, sh-XIST and miR-139 inhibitor were co-introduced into MLFCs; β-catenin and ECM protein levels were then determined by using assays. [score:2]
The functional role of miR-139 in XIST regulating β-catenin and ECM proteins. [score:2]
The indicated vectors were co -transfected into IMR-90 or MLFCs with miR-139 mimics, miR-139 inhibitor or sh-XIST, respectively; the luciferase activity was then determined by using dual luciferase assays. [score:2]
Results showed that miR-139 negatively regulated β-catenin protein levels (Figure 4E). [score:2]
These data indicated that miR-139 directly binds to XIST and β-catenin, respectively; XIST competes with β-catenin for miR-139 binding. [score:2]
Taken together, we revealed the promotive effect of XIST on BLM -induced PF, and demonstrated the mechanism by which XIST/miR-139 axis exerts its effect on regulating pulmonary fibrosis, providing a potential therapy to treat PF. [score:2]
These data indicated that miR-139 is involved in XIST regulating PF; miR-139 can partially reverse the effect of XIST on PF. [score:2]
Figure 6(A) and (B) miR-139 and β-catenin expression in PF and normal tissues were determined by using real-time PCR assays. [score:2]
MiR-139 and β-catenin expression in PF and normal tissues were determined by using real-time PCR assays. [score:1]
By performing Spearman’s rank correlation analysis, we observed an inverse correlation between miR-139 and XIST, between miR-139 and β-catenin, a positive correlation between XIST and β-catenin (Figure 6C, 6D and 6E). [score:1]
By using online tools, we found that XIST and β-catenin share an almost identical binding site of miR-139. [score:1]
We found that XIST shared an almost identical binding site of miR-139 with β-catenin by using online tools (Figure 4A and 4F). [score:1]
Figure 4(A) and (F) Online tools predicted that XIST and β-catenin shared an almost identical binding site of miR-139. [score:1]
These data suggested that XIST might compete with β-catenin for miR-139 binding during PF progression so as to repress the inhibitory effect of miR-139 on β-catenin, which inspired us to further investigate the detailed function of miR-139 in PF. [score:1]
XIST competed with β-catenin for miR-139 binding in IMR-90 and MLFCs. [score:1]
These all indicated that miR-139 might play a role in PF; XIST possibly exerts its function in promoting PF through competing with β-catenin for miR-139 binding. [score:1]
[1 to 20 of 37 sentences]
6
[+] score: 136
In the control network, let-7e-5p is linked to miR-139-5p, a candidate tumor suppressor targeting TIMELESS and found down-regulated in many cancer types, but in the tumor network this important link was lost. [score:8]
The potential relationship between TIMELESS and miR-139-5p was validated in our cohort of sporadic CRC patients, confirming the inverse expression pattern and suggesting that deregulation of this axis may play a role in disease progression. [score:6]
Besides, these miRNAs are involved in the pathways controlling cancer cell proliferation and invasiveness (Supplementary Table S6) Table 2 Fold Change (Tumor versus Control) Targets let-7e-5p Down PER1, CLOCK miR-125b-5p Down PER1, RORA, TIPIN miR-140-3p Down NPAS2, TIMELESS miR-99b-5p Down PER1, RORA, TIMELESS miR-19b-3p Up TIMELESS, NR1D2 miR-139-5p Down TIMELESS Figure 3 Multi-layer network of clock genes and targeting miRNAs in which nodes represent clock genes or miRNAs, while edges represent correlation or interaction among miRNAs or genes. [score:5]
In detail, miR-139-5p inhibition resulted in TIMELESS overexpression in HCT116 and HT29 with respect to SW480 and SW620, while no statistically significant variation was observed in CaCo2 cells. [score:5]
Interestingly, as reported in Supplementary Table S3, miR-139-5p was down-regulated and ranked among the most deregulated miRNAs in tumor tissues (False Discovery Rate = 0.002668, Fold Change = −6.801375, p value = 0.000013). [score:5]
CaCo2, HCT116, HT29, SW480 and SW620 cells at 70–80% confluence were transiently transfected with synthetic miR-139–5p mimic (MSY0000250, QIAGEN) or miR-139-5p inhibitor (MIN0000250, QIAGEN) or the appropriate scrambled controls (AllStar or mirScript Inhibitor-Negative Control) using HiPerfect Transfection Reagent (QIAGEN; Hilden, Germany), following the manufacturer's instructions. [score:5]
Consistently, miR-139-5p overexpression or inhibition induced higher or lower pre-apoptosis and apoptosis than basal cells, respectively (Figure 7B). [score:5]
Besides, these miRNAs are involved in the pathways controlling cancer cell proliferation and invasiveness (Supplementary Table S6) Table 2 Fold Change (Tumor versus Control) Targets let-7e-5p Down PER1, CLOCK miR-125b-5p Down PER1, RORA, TIPIN miR-140-3p Down NPAS2, TIMELESS miR-99b-5p Down PER1, RORA, TIMELESS miR-19b-3p Up TIMELESS, NR1D2 miR-139-5p Down TIMELESS Figure 3 Multi-layer network of clock genes and targeting miRNAs in which nodes represent clock genes or miRNAs, while edges represent correlation or interaction among miRNAs or genes. [score:5]
Finally let-7e-5p lost the link with miR-139-5p, an important tumor suppressor found deregulated in different cancer types [39– 43]. [score:4]
In contrast, re -expression of miR-139-5p in in vitro assays inhibited cell migration in all five cell lines examined. [score:4]
miR-139-5p negatively regulates TIMELESS expression in human colon cancer cell lines. [score:4]
Figure 5miR-139-5p negatively regulates TIMELESS expression in human colon cancer cell lines(A) The bar plot reports miR-139-5p and TIMELESS mRNA levels evaluated by qRT-PCR analysis in the indicated cell lines with respect to the average expression detected in non-tumor tissues. [score:4]
To investigate this possibility we assessed the effects of TIMELESS down-regulation upon miR-139-5p ectopic expression on colon cancer cell proliferation, apoptosis, migration and colony forming efficiency. [score:4]
miR-139-5p inhibits cell proliferation and apoptosis in human colon cancer cells lines. [score:3]
In fact, restoration of miR-139-5p significantly inhibited cell proliferation and apoptosis as evidenced by cell count and FACS analysis. [score:3]
These data were corroborated by the examination of TIMELESS and miR-139-5p expressions values of COAD and healthy tissues downloaded from the TCGA data portal, as preprocessed and normalized probeset intensity values (level 3). [score:3]
was performed as previously reported [58] CaCo2, SW480 and SW620 cells were transfected with miR-139-5p mimic or inhibitor or Controls 48 h at 37°C. [score:3]
Modulation of miR-139-5p expression through mimic or antisense RNAs induced remarkable and inverse variations of TIMELESS in CRC cells. [score:3]
Figure 7(A) Graphical representation of cell numbers assessed by automatic cell counting at different time points (24, 48 and 72 hrs) from transfection with the miR-139-5p mimic, miR-139-5p inhibitor, or the appropriate scrambled controls. [score:3]
TIMELESS mRNA was inversely correlated with miR-139-5p expression by a Pearson's correlation test (r = −0.320; p = 0.027) (Figure 4 upper panel). [score:3]
Finally, based on the expression levels and on topological considerations of miRNAs and clock genes, we selected miR-139-5p and TIMELESS to be further validated, in vitro, in a new cohort of CRC patients and in human colon cancer cell lines. [score:3]
Indeed, miR-139-5p expression displayed an opposite pattern to TIMELESS, with lower levels in all the examined cell lines than non-tumor mucosa; lower levels were detected in CaCo2 and HT29 with respect to HCT116, SW480 and SW620 cells (Figure 5A). [score:3]
No statistically significant difference was found for survival rates in a Kaplan–Meier analysis of censored data after stratifying patients according to the median expression value of TIMELESS mRNA (Log Rank–Mantel-Cox test p = 0.721) and miR139-5p (Log Rank-Mantel-Cox test p = 0.515) (Supplementary Figure S1). [score:3]
Expression levels of miR-139-5p were normalized to RNU6B and relative expression levels were calculated within each independent experiment using the formula 2 [−ΔΔCT]. [score:3]
Quantitative real-time PCR (qRT-PCR) assay was used to assess the differential expression of the TIMELESS gene and miR-139-5p in CRC specimens matched to normal mucosa. [score:2]
Median values, 25th (or first quartile, Q1) and 75th percentile (or third quartile, Q3) of GAPDH-Ct value/target gene- C [t] value are shown in Figure 4. Compared to matched non-tumor tissues a statistically significant increase of TIMELESS mRNA (median = 1.25, Q1-Q3 = 0.87-2.13, p < 0.001) and a decrease of miR-139-5p levels (median = 0.15, Q1–Q3 = 0.06–0.44, p < 0.0001) was observed in tumor tissues. [score:2]
miR-139-5p regulates proliferation, migration, colony forming efficiency and apoptosis in human colon cancer cell lines. [score:2]
Colony forming efficiency and migration assays were severely reduced in all CRC cell lines examined (p < 0.05 and p < 0.01) upon miR139-5p mimic ectopic expression. [score:2]
Western blot analysis on extracts from the same cells showed higher levels of the protein in CaCo2, HCT116 and in particular SW620 cells, suggesting a key role played by miR-139-5p in TIMELESS post-transcriptional regulation (Figure 5B). [score:2]
Apoptosis assay was performed as previously reported [58] CaCo2, SW480 and SW620 cells were transfected with miR-139-5p mimic or inhibitor or Controls 48 h at 37°C. [score:2]
In contrast, transfection of a miR-139-5p mimic down-regulated TIMELESS in all cells lines under investigation (Figure 5D). [score:2]
Figure 8(A) Plate colony-forming assay performed in the indicated cell lines transfected with miR-139-5p mimic or inhibitor or relative miRNA controls and stained with crystal violet (left panel); the histogram reports the value of colonies areas (right panel). [score:2]
These data confirm that miR-139-5p inversely correlates with TIMELESS regulating its protein levels in human colon cancer cells. [score:2]
Computational prediction of miR-139-5p seed regions on TIMELESS mRNA. [score:1]
TIMELESS mRNA and miR-139-5p levels are inversely correlated in sporadic colorectal cancer. [score:1]
Association of TIMELESS mRNA and miR-139.5p levels with clinical and pathological features of colorectal cancer patients included in the validation cohort. [score:1]
miR-139-5p recognizes two seed regions in TIMELESS mRNA and we decided to select this miRNA/gene pair for validation in an independent cohort of patients and, then, for in vitro functional studies. [score:1]
Putative miR-139-5p binding sites in TIMELESS mRNA were predicted by the RNAHybrid (http://bibiserv. [score:1]
Transfection efficiency was estimated by qRT-PCR evaluating miR-139-5p vs RNU6B expression levels. [score:1]
TIMELESS and miR-139-5p levels are inversely related in human colon cancer cell lines. [score:1]
The expression levels of TIMELESS mRNA and miR-139-5p were evaluated in the tumor tissues and adjacent non-tumor mucosa of an independent cohort of 50 CRC patients (34 men and 16 women, mean age ± SD 67.2 ± 11.6 years), surgically treated for colon and rectum primary tumors at our Hospital. [score:1]
Bioinformatic analysis identified two seed regions for miR-139-5p in the CDS and 3′UTR of TIMELESS mRNA, respectively (Figure 5C). [score:1]
Lower miR-139-5p levels were associated with a non-mucinous adenocarcinoma histologic type (p = 0.035) and high microsatellite instability frequency (p = 0.035) (Table 3). [score:1]
Figure 4 TIMELESS mRNA and miR-139-5p levels are inversely correlated in sporadic colorectal cancerBox-plot analysis of TIMELESS mRNA and miR-139-5p levels in our colorectal cancer (CRC) patients validation cohort (upper panel) and in the COAD-TCGA dataset (lower panel); p value and r coefficient of correlation are reported in the panels. [score:1]
Clinical-pathological features of CRC patients and association with TIMELESS mRNA and miR-139-5p levels. [score:1]
miR-139-5p reduces the colony forming area and cell invasion in human colon cancer cells lines. [score:1]
We quantified TIMELESS mRNA and miR-139-5p levels in 50 matched pairs of tumor tissues/non-tumor mucosa sampled from 46 well-moderately differentiated (G1-G2) and from 4 poorly differentiated-undifferentiated (G3-G4) CRCs. [score:1]
In contrast, the miR-139-5p antisense induced higher migration in HT29 and SW480 cells and, in these latter ones, also larger colonies (Figure 8A and 8B). [score:1]
Box-plot analysis of TIMELESS mRNA and miR-139-5p levels in our colorectal cancer (CRC) patients validation cohort (upper panel) and in the COAD-TCGA dataset (lower panel); p value and r coefficient of correlation are reported in the panels. [score:1]
TIMELESS MRNA AND MIR139-5P LEVELS ARE ALTERED AND INVERSELY CORRELATED IN SPORADIC CRCS. [score:1]
A time -dependent reduction of proliferation was observed in all cell lines upon miR-139-5p mimic transfection (p < 0.05); the reduction trend was less evident in HT29 cells (Figure 7A). [score:1]
In contrast, due to the low basal miR-139-5p levels in all cell lines, a miR-139-5p antisense increased the proliferation rate only in HT29 cells (p < 0.05). [score:1]
Furthermore, bioinformatic analysis identified miR-139-5p seed regions in the CDS and 3′UTR of TIMELESS mRNA, which plays a key role in DNA damage response, telomere length and integrity maintenance, cell cycle progression as well as processes coordinated at the DNA replication fork such as DNA synthesis, S-phase -dependent checkpoint activation and chromosome cohesion [44– 47]. [score:1]
This was further corroborated in a series of human colon cancer cell lines in which miR-139-5p induced TIMELESS down-modulation, determining the cell phenotype. [score:1]
[1 to 20 of 54 sentences]
7
[+] score: 44
Among the nine T-cell miRNAs affected by TNF-α and downregulated in RA T cells, the expression levels of miR-139-3p, miR-204, miR-214, and miR-760 were increased in patients using biologic agents. [score:6]
Each scatter spot representing average normalized expression level of miRNA in three repeats of each treatment; (b) 13 miRNAs exhibiting aberrant expression in Jurkat cells cultured with TNF-α (20 ng/mL) for 7 days; (c) decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 in RA T cells miRNA, compared with normal T cells. [score:6]
The expression levels of 12 miRNAs, including miR-139-3p, miR-204, miR-760, miR-432, miR-524-5p, miR-136, miR-548d-3p, miR-206, miR-214, miR-383, miR-224, and miR-887 were significantly lower, whereas the expression level of miR-146a was significantly higher, in Jurkat cells after being cultured with TNF-α for 7 days (fold change > 4, p < 0.05, Fig.   1b). [score:5]
Initially, our studies showed that among the expression of T cell miRNAs affected by TNF-α in Jurkat cells, the expression levels of miR-139-3p, miR-204, miR-760, miR-383, miR-524-5p, miR-136, miR-548d-3p, and miR-214 were significantly decreased in RA T cells. [score:5]
The expression levels of miR-139-3p, miR-204, miR-214, and miR-760 increased in RA patients using biologic agents. [score:3]
After adjusting for age and sex using multiple linear regression analysis (Table  2), RA patients with RF positivity had a significant 0.33-fold decrease (p = 0.039; 95% confidence interval [CI] 0.12–0.94) and the use of biologic agents had a significant 2.84-fold increase (p = 0.039; 95% CI 1.06–7.64) in miR-139-3p expression levels. [score:3]
Expression levels of miR-139-3p, miR-204, miR-214, and miR-760 were correlated with the use of biologic agents. [score:3]
The expression levels of miR-139-3p, miR-204, miR-214, and miR-760 increased in RA patients receiving biologic agents. [score:3]
With simple linear regression analysis, expression levels of miR-139-3p showed a significant correlation with rheumatoid factor (RF) positivity and the use of biologic agents. [score:3]
Decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 were noted in RA T cells. [score:3]
The expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 was found to be significantly lower in RA T cells (p < 0.05), compared with controls (Fig.   1c). [score:2]
The fold changes of expression levels for these miRNAs were 0.42-fold for miR-139-3p, 0.43-fold for miR-204, 0.13-fold for miR-760, 0.32-fold for miR-524-5p, 0.45-fold for miR-136, 0.19-fold for miR-548d-3p, 0.37-fold for miR-214;0.36-fold for miR-383, and 0.14-fold for miR-887, compared with controls. [score:2]
[1 to 20 of 12 sentences]
8
[+] score: 43
Thus, up-regulation of miR-425, miR-454 and miR-301a and down-regulation of miR-10b* and miR-139-5p were definitively confirmed. [score:7]
Among these miRs, we identified two (miR-10b* and miR-139-5p) that were down-regulated and three (miR-425, miR-454 and miR-301a) that were up-regulated for all three subtypes (Fig 1D and E and Supporting Information Fig S1A). [score:7]
To elucidate the biological significance of the down-regulation of miR-10b* and miR-139-5p in breast cancer, we analysed potential correlations between their expression and commonly known clinical attributes. [score:6]
No differences were observed in the miR-139-5p-over -expressing population (Fig 3D). [score:3]
A. Box-plots of the expression levels of miR-10b* and miR-139-5p for tumours of different sizes (pT1 < pT2 < pT3). [score:3]
No significant effects of miR-139-5p expression on the cell cycle were observed either in MDA-MB-468 or in MCF7 cells (Fig 3E and H). [score:3]
We next analysed the effect of miR-10b* or miR-139-5p expression on cell-cycle distribution by flow cytometry. [score:3]
No significant variation was found in cells over -expressing miR-139-5p (Fig 3B and C). [score:3]
To investigate whether the down-regulation of miR-10b* and miR-139-5p could be attributable to hypermethylation events occurring during breast carcinogenesis, we first examined the genomic loci of miR-10b* and miR-139-5p for the presence of CpG islands (Supporting Information Fig S2A and S2B). [score:2]
There was almost no effect of the treatment on the analysed miR-139 CpG island (Fig 2C). [score:1]
Figure 2 A. Schematic representation of the miR-10b and miR-139-5p genomic loci. [score:1]
Immunoprecipitated genomic DNA from MCF7 cell line was quantified by using qPCR with TaqMan assays directed to miR-10b* CpG islands #1 and #2 and miR-139-5p CpG Island #1. C. MeDIP experiment of MCF7 cells treated with 5-aza-dC. [score:1]
A. Schematic representation of the miR-10b and miR-139-5p genomic loci. [score:1]
Very low levels of methylation were observed on the CpG island upstream of miR-139-5p (Fig 2B). [score:1]
Growth curves of MDA-MB-468 (B) and MCF7 (C) cells transfected with miR-10b* (MIM 10b*) or miR-139-5p (MIM 139-5p) or control mimic (CTRL) were performed harvesting the cells after 24, 48 and 72 h from transfection. [score:1]
[1 to 20 of 15 sentences]
9
[+] score: 38
To understand the role of immunological and genetic factors involved in the transition of brucellosis into chronic infection, target pathway prediction of miR-1238-3p, miR-494, miR-6069, and miR-139-3p was performed according to KEGG function annotations, which increased miRNA (miR-1238-3p) of target genes involved in immunologically effective pathways as shown in Figure 2. miRNAs (miR-494, miR-6069, and miR-139-3p) that were downregulated in the chronic group were considered common. [score:7]
To understand the role of immunological and genetic factors involved in the transition of brucellosis into chronic infection, target pathway prediction of miR-1238-3p, miR-494, miR-6069, and miR-139-3p was performed according to KEGG function annotations, which increased miRNA (miR-1238-3p) of target genes involved in immunologically effective pathways as shown in Figure 2. miRNAs (miR-494, miR-6069, and miR-139-3p) that were downregulated in the chronic group were considered common. [score:7]
miR-1238-3p was upregulated, while miR-494, miR-6069, and miR-139-3p were downregulated in the chronic group compared with the active group. [score:6]
Downregulated microRNAs, miRNA-494, and miR-139-3p have been proven to be involved in the carcinogenesis and development of various types of cancer in previous studies [75– 80]. [score:5]
In the present study, we uniquely determined that reduced expression of miR-139-3p, miR-6069, and miR-494 and induced expression of miR-1238-3p were significantly associated with chronic brucellosis. [score:5]
The predicted number of target genes is present in Figure 4.183 genes (3%) were regulated mutually by miR-494, miR-139-3p, and miR-6069. [score:4]
Mutual KEGG pathway analysis of miR-494, miR-139-3p, and miR-6069 revealed that pathways related to these miRNAs in brucellosis have biological significance associated with the conversion of chronicity, including endocytosis, regulation of actin cytoskeleton, MAPK signaling pathway, cytokine-cytokine receptor interaction, and chemokine signaling pathways. [score:2]
miR-139-3p was also linked to endocytosis, regulation of actin cytoskeleton, cytokine-cytokine receptor interaction, MAPK signaling pathway, chemokine signaling pathway, cell adhesion molecules, phagosome, T cell receptor signaling pathway, leukocyte transendothelial migration, and bacterial invasion of epithelial cells pathways. [score:2]
[1 to 20 of 8 sentences]
10
[+] score: 30
Interestingly, from these 17 significant pairs (adjusted p-value ≤ 0.05) several downregulated tumour-suppressor miRNAs (e. g., miR-let-7c, miR-139, miR-145 or miR-195) appeared to regulate oncogenic genes related to the cell cycle and DDR pathways (BUB1B, AURKA, BIRC5, CENPK, BRCA1 and CHEK1). [score:7]
Conversely, tumour suppressor miRNAs (miR-145, miR-139 and miR-195) are the most strongly down-regulated miRNAs in our dataset. [score:6]
Most of these interactions involved cell cycle related genes, like SPC24 and CDC20 (regulated by the anti-oncomiR miR-139), and PKMYT1 (regulated by the tumour suppressor miR-195). [score:5]
Conversely, the anti-oncomiRs miR-145, miR-139 and miR-195 were the most strongly down-regulated miRNAs in our dataset. [score:4]
Moreover, miR-195 and miR-139 are also well-known tumour suppressor miRNAs 28. [score:3]
It is worthy to mention that its regulating miRNA (miR-139-5p) has been itself associated to prognosis in lung cancer 57 but again not in breast. [score:2]
An illustrative example is the SCP24/miR-139 couplet, where involvement of the individual components is well-established (SPC24 and miR-139-5p 45 46, while no experimental evidence is available for the pair. [score:1]
In the DNA replication pathway, the interaction of the MCM2 gene with the anti-oncomiR miR-139 was notable in the majority of tumours. [score:1]
The senescence pathway was also represented and while most of the associations identified were known, novel ones were found like HMGA2/miR-139 and EZH2/miR-195. [score:1]
[1 to 20 of 9 sentences]
11
[+] score: 29
The microarray results showed that the most upregulated expression changes were noticed for miR-139, miR-2469, and miR-486, while the highest downregulation was observed for miR-9, miR-29b, and miR-31 (Table  2). [score:9]
Moreover, miR-139-5p was also shown to induce cell cycle arrest (prerequisite of differentiation) by targeting oncogenic nuclear receptor subfamily 5, group a, member 2 (Nr5a2) [40], which was confirmed to be developmentally regulated in bovine skeletal muscle [41]. [score:5]
It is plausible that miR-139 supports the miR-486 -dependent inhibition of Foxo1 translation, thereby increasing the mTOR -mediated protein synthesis. [score:5]
Hasseine et al. [39] found that miR-139 directly targets Foxo1 mRNA and reduces the level of its protein. [score:4]
Among them is miR-139, which was expressed over 120 times more in the HER/LIM cells (Table 2, Fig. 4). [score:3]
Further, we assume that, at least partially, the coordinated action of miR-128 and miR-139 could influence the HER/LIM cell differentiation in a similar manner, possibly via the inhibition of Foxo1 and Nr5a2. [score:3]
[1 to 20 of 6 sentences]
12
[+] score: 24
Cells were transfected by separated with 25 μM of miR100-5p (overexpressed in all exosomes), miR21-5p (overexpressed in bulk cell exosomes) and miR139-5p (overexpressed in CSCs exosomes). [score:7]
The highly expressed hsa-miR-100-5p and hsa-miR-21-5p, and the differentially expressed hsa-miR-139-5p and hsa-miR-30c-5p, were detected in bulk cells and CSCs, and also in their exosomes. [score:5]
miR-100 also increased MMP-2 and -13 but it had no effect on MMP-9. miR-139 also regulated the expression of all MMPs. [score:4]
Transfection with miR-100, miR-21 and miR-139 increased significantly the expression of RANKL in fibroblasts at protein (Figure 7A and 7C) and mRNA levels (Figure 7B) that could act as a paracrine factor for cancer cells. [score:3]
Six of them were overexpressed in CSCs exosomes: hsa-miR-7641, hsa-miR-148a, hsa-miR-1307-3p, hsa-miR-183, hsa-miR-139 and hsa-miR-1307-5p. [score:3]
Then, cells were transfected separately with the miRNAs miR-100, miR-21 and miR-139. [score:1]
Finally, for the new targets genes prediction the mirMap bioinformatics software [73] was utilized with a pValue threshold of 0.01. cDNA was synthetized from miRNA samples (300 ng) from exosomes and cells with the TaqMan [®] MicroRNA Reverse Transcription Kit (Lifetechnologies) using a pool of primers included in the TaqMan miRNA assays for hsa-miR-100, hsa-miR-21-5p, hsa-miR-139-5p, hsa-miR-30c and U6 snRNA according to manufacturer's instructions. [score:1]
[1 to 20 of 7 sentences]
13
[+] score: 24
Dysregulation of MIR101, MIR141, and MIR152 to the HIV-1 Gag protein contributes to HIV-1 budding and release via DNA hypermethylation, ubiquitin transfer, and endoplasmic reticulum -associated degradation at the late infection stage Briefly, dysregulation of; dysregulation of MIR9 contributes to HIV-1 infection to hijack CD4+ T cells through dysfunction of the immune and hormone pathways; dysregulation of MIR139-5p, MIRLET7i, and MIR10a contributes to the HIV-1 integration/replication stage through DNA hypermethylation and immune system dysfunction; dysregulation of MIR101, MIR141, and MIR152 contributes to the HIV-1 virus assembly/budding stage through DNA hypermethylation, ubiquitin transfer, and endoplasmic reticulum -associated degradation; dysregulation of MIR302a contributes to not only microvesicle -mediated transfer of miRNAs but also dysfunction of NF-κB signaling pathway in hepatocarcinogenesis. [score:7]
At the intermediate HIV infection stage, we identified that the expression change of MIR139-5p (p-value < 0.23) contributes to the expression change of DDX3X (p-value < 0.14) via miRNA regulation (p-value < 1☓10 [-16]). [score:6]
We found that dysregulation of; dysregulation of MIR9 contributes to HIV-1 infection to hijack CD4+ T cells through dysfunction of the immune and hormone pathways; dysregulation of MIR139-5p, MIRLET7i, and MIR10a contributes to the HIV-1 integration/replication stage; dysregulation of MIR101, MIR141, and MIR152 contributes to the HIV-1 virus assembly and budding mechanisms; dysregulation of MIR302a contributes to not only microvesicle -mediated transfer of miRNAs but also dysfunction of NF-κB signaling pathway in hepatocarcinogenesis. [score:6]
Therefore, we suggested that DDX3X could regulate HIV replication through MIR139-5p regulations [98, 99]. [score:3]
Dysregulation of MIR139-5p contributes to HIV-1 replication via DNA hypermethylation. [score:2]
[1 to 20 of 5 sentences]
14
[+] score: 21
Sixteen of 359 miRNAs detected were differentially expressed between tumor and matched benign tissue (adjusted p < 0.05): 9 were upregulated (hsa-miR-19a; hsa-miR-512-3p; hsa-miR-27b; hsa-miR-20a; hsa-miR-28-3p; hsa-miR-200c; hsa-miR-151-3p; hsa-miR-223; hsa-miR-20b), and 7 downregulated (hsa-miR-22; hsa-miR-516-3p; hsa-miR-370; hsa-miR-139-5p; hsa-let-7e; hsa-miR-145-3p; hsa-miR-30c) in tumor tissue in comparison to matched benign tissue (Table 2). [score:9]
Of the seven tumor-tissue miRNAs downregulated, four (hsa-miR-370; hsa-miR-139-5p; hsa-miR-let-7e; hsa-miR30c) were expressed in both tumor and plasma (both free and within exosomes); hsa-miR-516-3p was present in tumor only, and hsa-miR-22 and hsa-miR-145-3p were present in tumor and exosome only. [score:6]
miRNA Expression Cancer association (Y/N) Upregulated (Y/N) hsa-miR-19a Common YY (10) hsa-miR-512-3p T and E only YN (11) hsa-miR-27b Common YY (12) and N (13) hsa-miR-20a Common YY (14) hsa-miR-28-3p Common YY (15) hsa-miR-200c Common YY (16) and N (17) hsa-miR-151-3p Common YY (18) hsa-miR-223 Common YY (19) and N (15) hsa-miR-20b Common YY (20) hsa-miR-22 T and E only YY (19, 21) and N (22) hsa-miR-516-3p T only N N/A hsa-miR-370 Common YY (23) hsa-miR-139-5p Common YN (24) hsa-let-7e Common YN (25) hsa-miR-145-3p T and E only YN (26) hsa-miR-30c Common YN (27) T, tumor; E, exosome. [score:6]
[1 to 20 of 3 sentences]
15
[+] score: 21
Notably the microRNAs upregulated in the control fascia accounting for the greatest differential in read count are heavily enriched in previously validated anti-fibrotic extracellular matrix targeting microRNAs (Table  1), including let-7 [23– 25], miR-29a-3p [26], miR-26b-5p, miR-30d-5p [27, 28], miR-27a-3p, miR-27b-3p [29, 30], miR-10a-5p [31], miR-26a-5p [32– 35], miR-101-3p [36– 39], and miR-10b-5p [40], as well as anti-proliferative microRNAs including, miR-126-3p [41– 47], miR-99a-5p [48– 54], miR-125a-5p [55– 59], and miR-139-5p [60– 62]. [score:6]
Luo HN Wang ZH Sheng Y Zhang Q Yan J Hou J Zhu K Cheng Y Xu YL Zhang XH Xu M Ren XY MiR-139 targets CXCR4 and inhibits the proliferation and metastasis of laryngeal squamous carcinoma cellsMed Oncol. [score:4]
Additional enriched microRNAs (miR-126-3p [46– 52], miR-99a-5p [53– 59], miR-125a-5p [60– 64], and miR-139-5p [65– 67]) have been shown to affect proliferation in cancer, and may regulate the fibroproliferative activity seen in Dupuytren’s disease. [score:4]
14 hsa-miR-127-5p 1708.96 hsa-miR-139-5p 1096.97 hsa-miR-146b-5p 1662.59 hsa-miR-23b-3p 1281.21 hsa-miR-193b-3p 1275.18 hsa-miR-320b 1148.60 hsa-miR-146a-5p 1135.37 hsa-miR-210 1055.20 hsa-miR-708-3p 1027.45 hsa-miR-769-5p 1004.10 hsa-miR-378d 1000.99 To determine if adjacent fascia exhibits a disease-like molecular phenotype, we compared the adjacent fascia biopsies with patient matched diseased Dupuytren’s fascia. [score:4]
Liu R Yang M Meng Y Liao J Sheng J Pu Y Yin L Kim SJ Tumor-suppressive function of miR-139-5p in esophageal squamous cell carcinomaPLoS One. [score:3]
[1 to 20 of 5 sentences]
16
[+] score: 19
In order to further understand the role of aberrant miRNAs in physiological functions and biologic processes in arsenite -induced neoplastic transformation cells, 11 downregulated miRNAs (miR-197-3p, miR-192-5p, miR-127-3p, miR-139-5p, miR-490-3p, miR-196b-5p, miR-125a-3p, miR-298, miR-542-3p, miR-15b-5p, and miR-33b-5p) and six upregulated miRNAs (miR-200b-3p, miR-106b-5p, miR-574-5p, miR-320d, miR-200c-3p, and miR-141-3p) (Table S2) were selected, and their target genes were predicted with the TargetMiner, miRDB, and TarBase databases. [score:11]
Among the 191 dysregulated miRNAs, seventeen miRNAs (downregulation miRNAs: miR-197-3p, miR-192-5p, miR-127-3p, miR-139-5p, miR-490-3p, miR-196b-5p, miR-125a-3p, miR-298, miR-542-3p, miR-15b-5p, miR-33b-5p; upregulation miRNAs: miR-200b-3p, miR-106b-5p, miR-574-5p, miR-320d, miR-200c-3p, miR-141-3p, Table S2) were selected for bioinformatics analysis. [score:8]
[1 to 20 of 2 sentences]
17
[+] score: 17
Other miRNAs from this paper: hsa-mir-182, hsa-mir-34c, hsa-mir-486-1, hsa-mir-4423, hsa-mir-486-2
The hsa-miR-486-3p, hsa-miR-182-5p, and hsa-miR-139-5p showed dose -dependent upregulation in fold expression value, whereas hsa-miR-34c-5p and hsa-miR-4423-3p remained twofold upregulated with no significant deviation in fold expression at all three test concentration. [score:11]
Moreover we also found upregulation in 5 miRNAs (has-miR-486-3p, has-miR-34c-5p, has-miR-4423-3p, has-miR-182-5p, and has-miR-139-5p) which play role in muscle contraction, Arginine and proline metabolism and Hypertrophic cardiomyopathy (HCM). [score:4]
In addition, we also identified 5 out of 14 miRNAs; hsa-miR-486-3p, hsa-miR-34c-5p, hsa-miR-4423-3p, hsa-miR-182-5p, and hsa-miR-139-5p deregulated after ETP treatment (Fig.   2e). [score:2]
[1 to 20 of 3 sentences]
18
[+] score: 16
miR-139-5p has been known to be a tumor suppressor miRNA by inhibiting the metastasis pathway [46]; however, miR-139-3p has not been well studied and is often neglected, since much literature has only used miR-139. [score:5]
In the down-regulated group, there are seven miRNA pairs (miR-139, miR-29c, miR-145, miR-378, miR-30a, miR-143 and miR-144) with both the 5p-arm and 3p-arm identified as significantly dys-regulated miRNAs. [score:5]
The down-regulated miRNAs include miR-139-5p, miR-139-3p, miR-145-5p, miR-145-3p, miR-486-5p, and miR-1-2-3p. [score:4]
Zhang H. D. Jiang L. H. Sun D. W. Li J. Tang J. H. miR-139-5p: Promising biomarker for cancer Tumour. [score:1]
There are few miRNA 5p-arm and 3p-arm pairs identified in our study: miR-21-5p and miR-21-3p; miR-141-5p and miR-141-3p; miR-139-5p and miR-139-3p; miR-145-5p and miR-145-3p. [score:1]
[1 to 20 of 5 sentences]
19
[+] score: 15
Analyses in vitro and in vivo have demonstrated miR-139-5p suppressed tumor growth and directly targeted MET, which could be a possible mechanism by which miR-139-5p regulates growth and the metastatic potential [70]. [score:7]
Dysregulated miR-139 expression has been reported in some human tumor types. [score:4]
The down-regulation of miR-451a, miR-144, miR-195, miR-218, miR-145, miR-30a, miR-126 and miR-139 has been found in both the training and validation set. [score:4]
[1 to 20 of 3 sentences]
20
[+] score: 15
Expression of miR-124 and miR-137, respectively, increased up to 8- and 24-fold, expression of miR-129 and miR-139, respectively, decreased up to 2- and 4-fold, and expression of miR-7 and miR-218 did not change appreciably. [score:7]
Of the 35 miRNAs, we identified six HGA-miRNAs, which were down-regulated in both AA and GBM tumors at a more stringent degree of significance (P < 0.01): miR-7, miR-124, miR-129, miR-137, miR-139 and miR-218. [score:4]
We identified six miRNAs of particular interest, miR-7, miR-124, miR-129, miR-137, miR-139 and miR-218, which were down-regulated in both AAs and GBMs (Figure 1A, Additional file 8 and Table 1) at a more stringent level of significance (P ≤ 0.01). [score:4]
[1 to 20 of 3 sentences]
21
[+] score: 15
mRNA, messenger RNA Table 1circRNA-miRNA-mRNA network elements for those circRNA-miRNA interactions predicted by both miRanda and RNAHybrid, with a miRanda match score > = 180 and mRNA targets that are differentially expressed (uncorrected P < 0.05) with log2(fold change) >= 2 or =< − 2 (high stringency network) Circular RNA microRNA target Number of binding sites predicted Target genes (differentially expressed) X:47,431,299–48,327,824 hsa-miR-139-5p 6 NOTCH1, STAMBP, TPD52 8:144,989,320–145,838,888 hsa-miR-320a 2 METTL7A, PBX3, PLS1, SEC14L1, VCL, VIM, VOPP1, YPEL2 8:144,989,320–145,838,888 hsa-miR-320b 2 RTKN, VCL, VOPP1 X:47,431,299–48,327,824 hsa-miR-449a 1 BAZ2A, MFSD8, NOTCH1, TSN, ZNF551 8:144,989,320–145,838,888 hsa-miR-125a-3p 1 ANKRD62, C15orf40, COL18A1, MFSD11, MPEG1, MUL1, TTC31, WDR12, ZNF641 X:47,431,299–48,327,824 hsa-miR-125a-5p 1 CD34, MEGF9, PANX1, RIT1, TP53INP1 8:144,989,320–145,838,888 hsa-miR-125a-5p 1 CD34, MEGF9, PANX1, RIT1, TP53INP1 X:47,431,299–48,327,824 hsa-miR-324-5p 1 FOXO1, MEMO1, PSMD4, SMARCD2 14:23,815,526–24,037,279 hsa-miR-142-3p 1 BTBD7, CLDN12, CPEB2, CSRP2, DAG1, KIF5B, PTPN23, WHAMM 4:88,394,487–89,061,166 hsa-miR-133b 1 FAM160B1 4:88,394,487–89,061,166 hsa-miR-448 1 DDIT4, PURG 4:88,394,487–89,061,166 hsa-miR-339-5p 1 AXL, HLA-E, METTL7A, ZNF285, ZNRF3 MetaCore pathway analysis on the 255 filtered differentially expressed target genes from the previous analysis revealed 112 perturbed pathways (corrected P < 0.01; Table  2, Additional file  8: Table S5). [score:15]
[1 to 20 of 1 sentences]
22
[+] score: 13
For the latent stage, 18 consistently differentially expressed mature miRNA sequences were identified: 8 were up-regulated (miR-212-3p, miR-21-5p, miR-132-3p, miR-20a-5p, miR-17-5p, miR-27a-3p, miR-23a-3p, miR-146a-5p) and 10 were down-regulated (miR-139-5p, miR-551b-3p, miR-33-5p, miR-708-5p, miR-7a-5p, miR-935, miR-138-5p, miR-187-3p, miR-30e-3p, miR-222-3p) (Table  2). [score:9]
The most common down-regulated miRNAs were miR-30a-5p (6 profiles), followed by miR-139-5p, miR-187-3p, miR-551b-3p, miR-140-3p, miR-324-5p, miR-33-5p, miR-218-5p, miR-378a-3p and miR-29c-5p (Supplementary Table  S4). [score:4]
[1 to 20 of 2 sentences]
23
[+] score: 13
A Mann-Whitney U test of miRNAs normalized to miR-99a-5p and miR-139-5p expressed in at least 5 of 7 fasting or 5 of 7 non-fasting samples showed that no miRNAs were significantly (P < 0.05) differentially expressed between the two groups (data not shown). [score:5]
A Mann-Whitney U test conducted on miRNAs normalized to miR-99a-5p and miR-139-5p and detected in at least 80% of smokers or 80% of non-smokers showed that no miRNAs were significantly (corrected P-value < 0.05) differentially expressed. [score:3]
After normalization to miR-99a-5p and miR-139-5p, Pearson correlation coefficients between serum triglyceride concentration and miRNA levels showed 6 miRNAs were significantly (4 directly and 2 inversely) correlated with serum triglyceride levels (Table  5). [score:2]
We propose that miR-99a-5p and miR-139-5p should be used for sample normalization instead of these commonly used endogenous controls due to the fact that they are not significantly affected by hemolysis and that they have the lowest standard deviation across a series of 154 samples (Table  3). [score:1]
Therefore, for the following analyses, all data were normalized to the average Ct values of miR-99a-5p and miR-139-5p. [score:1]
Taking the above results into consideration, we have identified miR-99a-5p and miR-139-5p as novel endogenous controls for serum miRNA studies due to their consistency across all sample sets. [score:1]
[1 to 20 of 6 sentences]
24
[+] score: 13
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Furthermore, we and Gorter et al. 24 observed the up-regulation of miR-17-5p, miR-20a-5p, miR-23a-3p and the down-regulation of miR-139-5p, whereas we and Bot et al. 23 observed the down-regulation of miR-551b-3p. [score:10]
Another subgroup of miRNAs displayed an opposite pattern, i. e. decreased expression during latency: miR-7a-1-3p, miR-107-3p, miR-138-5p, miR-139-3p, miR-186-5p, miR-204-5p, miR-222-3p, miR-324-3p and miR-505-3p were significantly decreased during latency (peak at 4 days after SE), then gradually returned to control levels (Fig. 2, Supplementary Fig. S2). [score:3]
[1 to 20 of 2 sentences]
25
[+] score: 12
Ectopic expression of miR-139-3p inhibited myeloid progenitor proliferation of myeloid progenitors, increased miR-199a-3p enhanced proliferation of progenitors and accelerated the AML phenotype. [score:5]
Although this study directly supports the role of miR-199a-3p as an onco-miRNA, it also indicates that an auto-regulatory negative feedback from the elevated miR-139-3p as a suppressor is involved in the defective hematopoietic function in ICL-caused AML. [score:5]
Studying AML caused by toxic DNA interstrand crosslinks (ICLs), Alemdehy et al [33] found that miR-139-3p and miR-199a-3p had opposite effects on hematopoiesis. [score:1]
In the study, both miR-139-3p and miR-199a-3p increased with age in myeloid progenitors from the nucleotide excision repair gene (Ercc1) -deficient mice. [score:1]
[1 to 20 of 4 sentences]
26
[+] score: 12
In particular, ssc-miR-139-5p and its putative target SLA-DQB1 were co-expressed in the three tissues, and ssc-miR-423-5p and its putative target RNF5 were co-expressed in Abdominal Fat and Longissimus Dorsi muscle. [score:9]
In particular, the miR-139-5p target site in SLA-DQB1 was conserved in HLA-DQB1, and we found a variant that disrupted this site in the pig. [score:3]
[1 to 20 of 2 sentences]
27
[+] score: 11
In our recent study, we have shown that reduced expression of miR-139-3p, miR-6069 and miR-494 and induced expression of miR-1238-3p were significantly associated with chronic brucellosis [43]. [score:5]
In our previous study, more than 2000 miRNAs were screened in peripheral blood mononuclear cells of patients with acute or chronic brucellosis and we determined that while the expression level of miR-1238-3p was increased, miR-494, miR-6069 and miR-139-3p were decreased in the chronic group in comparison to the acute infection group [43]. [score:3]
Altered expressions of miR-1238-3p, miR-494, miR-6069 and miR-139-3p in the formation of Chronic Brucellosis. [score:3]
[1 to 20 of 3 sentences]
28
[+] score: 11
Calin et al. reported that one of the most upregulated miRNAs is miR-106a, which is consistently reported in six studies, and the five most downregulated miRNAs are miR-30a-3p, miR-139, miR-145, miR-125a, and miR-133a, which are consistently reported and differentially expressed in four studies; these miRNAs may actually be of clinical use as diagnostic/prognostic biomarkers or therapeutic targets [3]. [score:11]
[1 to 20 of 1 sentences]
29
[+] score: 11
Other miRNAs from this paper: hsa-mir-125b-1, hsa-mir-125b-2
For example, miR-139 that targets ROCK2 [22] was frequently down-regulated in human HCC by EZH2 -mediated H3K27me3 [13]. [score:6]
Recently, we have also reported that EZH2 epigenetically inactivates expressions of multiple tumor and metastasis suppressor microRNAs (miRNAs), such as miR-125b and miR-139 in human hepatocellular carcinoma (HCC), thereby promotes HCC tumorigenicity and metastasis [13]. [score:5]
[1 to 20 of 2 sentences]
30
[+] score: 11
In previous studies, several miRNAs, such as miR-7 [11], miR-122 [12], miR-139 [13] and miR-375 [14] have shown therapeutic potential that can delay the progression and development of certain human cancers by epigenetically interfering of primary signalling by targeting IGF-1R. [score:4]
Shen K MiR-139 inhibits invasion and metastasis of colorectal cancer by targeting the type I insulin-like growth factor receptorBiochem. [score:4]
In particular, miR-122 [12], miR-139 [13] and miR-140 [15] targeting to IGF-1R gene play important key roles during tumourigenesis or metastatic spread in an in vivo mo del of various malignant cells. [score:3]
[1 to 20 of 3 sentences]
31
[+] score: 10
The other candidate EZH2 binding miRNAs displayed a very similar pattern of expression: for example, the expression kinetics of miR-139 was similar to that of miR-101, and the expression pattern of miR-31 and miR-200b was comparable to that of miR-138 throughout differentiation (S4 Fig). [score:7]
B. Relative expression of 8 microRNAs (miR-31, miR-98, miR-125, miR-139, miR-181a, miR-181b, miR-200b and miR-217) during hepatocytes differentiation from hPSC- iEZH2 cell line doxy induced the first 8 days of differentiation. [score:3]
[1 to 20 of 2 sentences]
32
[+] score: 9
REST directly down-regulates a large number of genes at the transcriptional level, but also probably indirectly activates the expression of other genes at the post-transcriptional level via the repression of many noncoding targets (Conaco et al., 2006; Mortazavi et al., 2006; Wu and Xie, 2006; Visvanathan et al., 2007; Singh et al., 2008; Johnson et al., 2009), including several micro RNAs (miRNAs) considered to be brain-specific (such as miR9, miR124, miR132, miR135, miR139, and miR153; Figure 1). [score:9]
[1 to 20 of 1 sentences]
33
[+] score: 9
One study showed that miR-139-5p secreted from primary prostate cancer cell cultures increased the expression of genes that can contribute to the invasive properties of PCa cell populations [55]. [score:3]
Runx1 is uniquely targeted by miR-139-5p and miR-382-5p, neither miRNA has been extensively examined in association with prostate cancer. [score:3]
To discover the molecular mechanisms through which Runx1, Runx2, and the Runx -targeting miRNAs, miR-23b-5p, miR-139-5p, miR-205-5p, miR-221-3p, miR-375-3p, miR-382-5p, and miR-384-5p, drive prostate tumorigenesis, we interrogated well-accepted bioinformatics tools; DAVID [57, 58] and Ingenuity Pathway Analysis (IPA-www. [score:3]
[1 to 20 of 3 sentences]
34
[+] score: 9
For instance, both infected S-NSC and S-NDC cells overexpressed mir-139, a microRNA that is overexpressed in the hippocampus of a mouse mo del for Alzheimer’s Disease (AD) and associated with impaired hippocampus -dependent learning and memory [57]. [score:7]
Tang, Y., Bao, J. S., Su, J. H. & Huang, W. MicroRNA-139 modulates Alzheimer’s -associated pathogenesis in SAMP8 mice by targeting cannabinoid receptor type 2. Genet Mol Res 16, doi:10.4238/gmr16019166 (2017). [score:2]
[1 to 20 of 2 sentences]
35
[+] score: 9
While downregulation of miR-139 has been observed in HNOC [25, 27], relative little is known of the relationship of miR-139 and cancer [99]. [score:4]
Also, downregulation of several microRNAs has been consistently observed in HNOC, including miR-26b, miR-138, miR-107, miR-139. [score:4]
More studies will be needed to define the role of miR-139 in tumorigenesis. [score:1]
[1 to 20 of 3 sentences]
36
[+] score: 9
It was recently demonstrated that EZH2 is frequently upregulated in primary HCCs, and miRNA expression profiling in HCC cells with EZH2-knockdown revealed that a set of miRNAs, including miR-139-5p, miR-125b, let-7c, miR-101, and miR-200b, are epigenetically suppressed by EZH2 in HCC (Au et al., 2012). [score:9]
[1 to 20 of 1 sentences]
37
[+] score: 8
Some example sentences in this category include: “miR-23b is epigenetically down-regulated and restoration of miR-23b can effectively suppress cell growth in glioma stem cells” or “miR-139-5p is a potential biomarker for early diagnosis and prognosis and is a therapeutic target for esophageal squamous cell carcinoma (ESCC)”. [score:8]
[1 to 20 of 1 sentences]
38
[+] score: 8
Of note, miR-185, miR-139-5p, miR-484, and miR-130b were down-regulated in obese without DM-2 when compared to non-obese subjects while the expression of miR-99a, miR-1229, miR-125b, miR-221 and miR-199a-5p was up-regulated [Figure 4A and Table S2]. [score:8]
[1 to 20 of 1 sentences]
39
[+] score: 7
The microRNA-139-5p has been reported to act as a tumor suppressor inhibiting ELTD1 expression in glioblastoma cell lines [15]. [score:7]
[1 to 20 of 1 sentences]
40
[+] score: 7
Altogether, both lymphoma subtypes had only eight common miRs: three that were upregulated (miR-210, 155 and miR-106a), and five that were downregulated (miR-139, 150, 149, 320 and miR-34a-5p) (Figure 2D). [score:7]
[1 to 20 of 1 sentences]
41
[+] score: 7
0181231.g001 Fig 1 (a) Search human miR-139-3p’s target genes which are expressed in the brain tissue, related to the brain neoplasms disease and supported by at least two existing databases. [score:7]
[1 to 20 of 1 sentences]
42
[+] score: 7
MiR-139-5p (p = 0.0006) targets IGF1R which together with PDK1 (a kinase downstream of IGF1R (both IGF1R and PDK1 are targeted by miR-375)) has been shown to be induced by light in a study of the coupling of cell proliferation with diurnal/circadian cycles in a human breast cancer mo del [51]. [score:5]
This study identified miR-99a-5p and miR-139-5p as novel endogenous controls for serum miRNA because of stable values across individuals. [score:1]
For miR-139-5p, the data in fact show clear rhythmicity (p = 0.0006). [score:1]
[1 to 20 of 3 sentences]
43
[+] score: 7
Interestingly, miR-139-5p, the most down-regulated in the T vs N comparison, has very recently been identified as a member of a signature predictive of the clinical aggressiveness of stage II CRC [29]; in addition, miR-224, the most up-regulated together with miR-183 in the same comparison, has been identified for its ability to distinguish CRC by means of proficient or deficient DNA mismatch repair machinery [30]. [score:7]
[1 to 20 of 1 sentences]
44
[+] score: 7
miRNA-139 is an IL-1β-inducible miRNA that displays a chondral lesion-specific pattern of expression in OA, which seems to stimulate cartilage matrix catabolic processes via positively regulating the expression of the enzymes MMP-13 and ADAMTS4. [score:6]
Additionally, miRNA-139 exerts pro-apoptotic effects in human OA chondrocytes [96]. [score:1]
[1 to 20 of 2 sentences]
45
[+] score: 7
When Sa/CD99 cells are terminally differentiated (day 14) [28], we observed a modulation of a different set of miRs: miR-342-3p was the most down-regulated, while miR-139-3p, miR-1288 and miR-1914* were the most up-regulated. [score:7]
[1 to 20 of 1 sentences]
46
[+] score: 7
Other miRNAs from this paper: hsa-mir-122, hsa-mir-185, hsa-mir-340, hsa-mir-486-1, hsa-mir-486-2
Through combined analyses from web -based miRNA resources (miRanda and TargetScan), we identified 6 top candidate miRNAs that might regulate ITGB5 expression, including miR-122, miR-486-5p, miR-139, miR-340, miR-271, and miR-185 (Fig.   5a). [score:6]
b The 3′UTR of ITGB5 was constructed into a pSICHECK2 vector and was cotransfected with miR-122, miR-486-5P, miR-139,miR-271 and miR-185 individually. [score:1]
[1 to 20 of 2 sentences]
47
[+] score: 7
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-141, hsa-mir-200c, hsa-mir-200a, hsa-mir-429
More recently, we have further demonstrated that the frequent up-regulation of ROCK2 was partially contributed by the loss of expression of its regulatory miRNA, miR-139 [17]. [score:7]
[1 to 20 of 1 sentences]
48
[+] score: 7
Compared to normal tissue with an expression profile normalized to 1, in tumor samples of the 14 CRC patients we observed a significant up-regulation for 3 miRNAs (miR-31, miR-21 and miR-708), and under expression in 7 others (miR-145, miR-139-5p, miR-486-5p, miR-378, miR-140-3p, miR-143 and miR-30c) (Table 3). [score:7]
[1 to 20 of 1 sentences]
49
[+] score: 7
miR-522, miR-139-3p, miR-520c-5p, miR-518d-5p, miR-146b-5p, miR-34a, miR-526a, miR-193a-3p, miR-221, miR-4674 were significantly upregulated and miR-760 was downregulated in ECSCs (Figure 2A). [score:7]
[1 to 20 of 1 sentences]
50
[+] score: 7
For instance, in cytotoxic T lymphocytes (CTL), IL-2R and inflammatory signals act through Dicer and miRNAs to control the cytolytic program and CTL differentiation, in which miR-139 and miR-150 are downregulated by inflammation in CTLs, and miR-150 regulates the expression of the IL-2 receptor α-chain (CD25) [52]. [score:7]
[1 to 20 of 1 sentences]
51
[+] score: 6
Downregulation of miR-139 improves the invasive capacity of HCC cells in vitro and HCC metastasis in vivo [75]. [score:4]
MiR-139 interacts with Rho-kinase 2 (ROCK2) and reduces its expression in HCC cells line. [score:2]
[1 to 20 of 2 sentences]
52
[+] score: 6
Five miRNAs were upregulated (miR-130b, miR-182, miR10b, miR320a, and miR769) ranging from a 2.9 to 30-fold induction in the NanoString miRNA assay, whereas six miRNAs were downregulated (miR122, miR451a, miR200a, miR139, miR148a, and miR375) ranging from −2.2 to −6 fold (Table  6). [score:6]
[1 to 20 of 1 sentences]
53
[+] score: 6
As a result, we identified the expression levels of five miRNAs, including let-7e, miR-204, miR-216b, miR-9, and miR-139-5p as significantly downregulated in the PVD group, as shown by lower -ΔCT values (Fig 1C and 1D). [score:6]
[1 to 20 of 1 sentences]
54
[+] score: 6
Because we happened to measure 4 other miRNAs among the 16 miRNA biomarkers reported by Wan et al. (miR-30a-5p, miR-33a-5p, miR-139-5p, and miR-451a), we further examined the levels of these miRNAs in subject #7. Interestingly, all 4 miRNAs showed the same up- or down-regulation expression pattern as reported by Wan et al. Therefore, it is tempting to speculate whether emotional status of subject #7 affected the miRNA expression level in CSF. [score:6]
[1 to 20 of 1 sentences]
55
[+] score: 6
Li Q miR-139-5p inhibits the epithelial-mesenchymal transition and enhances the chemotherapeutic sensitivity of colorectal cancer cells by downregulating BCL2Sci. [score:6]
[1 to 20 of 1 sentences]
56
[+] score: 6
Recently, Au et al. (2012) analyzed the changes in miRNA expression profiles induced by EZH2 knockdown and found that some tumor-suppressive miRNAs (mir-139, -125b, -101, - 200b, and let-7c) are silenced by H3K27me3 in hepatocellular carcinoma. [score:6]
[1 to 20 of 1 sentences]
57
[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
In a review, Gramantieri et al. (2008) show miRNAs aberrantly expressed in HCC compared to non-tumorous liver tissue (up -expression of miR-33, miR-130, miR-135a, miR-210, miR-213, miR-222, miR-331, miR-373, miR-376a, and down -expression of miR-130a, miR-132, miR-136, miR-139, miR-143, miR-145, miR-150, miR-200a, miR-200b, miR-214). [score:6]
[1 to 20 of 1 sentences]
58
[+] score: 6
The dsyregulation of miRNAs in HCC have been reported using miRNA expression profiling studies with several miRNAs reported as enhancers (miR-30d, miR-151, miR-210) or suppressors (miR-122, let-7g, miR-29b, miR-193b, miR-194, miR-139 and miR-124) of the metastatic process [8]. [score:6]
[1 to 20 of 1 sentences]
59
[+] score: 5
Synthetic miRNA precursors – pre-miR-132, pre-miR-139 and pre-miR-526b (Table S2) – were transfected to HeLa cells or were treated with recombinant Dicer in a suitable buffer (Figure 1). [score:1]
Using the pre-miRNA 5′-arm specific probes, we could detect the miRNAs that were generated by the RNase IIIb domain of Dicer from pre-miR-526b and pre-miR-139, and using the 3′-arm specific probe, we detected miRNAs generated by the RNase IIIa domain of Dicer from pre-miR-132 (Figure 4A). [score:1]
0028548.g004 Figure 4(A) of RNA from in vitro reaction (line ‘DICER’) and cellular RNA (line in ‘cell’) with probes specific for miRNA derived from the 5′-arm of pre-miR-526b and pre-miR-139 and the 3′-arm of pre-miR-132. [score:1]
The black bar on the right side marks the miRNA and pre-miRNA fractions; (B) The same as in A, but antisense probes for miR-139 (3′-arm) and miR-132 (5′-arm) were used; (C) Northern blotting analysis with probes detecting miRNA derived from the 3′-arms of precursors after transfection of HeLa cells with vectors encoding pri-miR-137 and pri-miR-206. [score:1]
The pre-miRNAs used for transfection, pre-miR-132, pre-miR-136, pre-miR-139 and pre-miR-526b, were chemically synthesized (Curevac) and purified by polyacrylamide gel electrophoresis. [score:1]
[1 to 20 of 5 sentences]
60
[+] score: 5
Three among them, miR-101, miR-125b and miR-139-5p have been confirmed as targets of EZH2 [17, 25]. [score:3]
Three among them, miR-101, miR-125b and miR-139-5p have been confirmed as targets of EZH2 by ChIP assays [17, 25]. [score:2]
[1 to 20 of 2 sentences]
61
[+] score: 5
Other miRNAs from this paper: hsa-mir-18a, hsa-mir-26a-1, hsa-mir-31, hsa-mir-195, hsa-mir-26a-2
Among lncRNAs, lnc00152 has been reported to play an oncogenic role in promoting gastric cancer cell growth, migration, and invasion and in suppressing cell apoptosis by sponging miR-18a-5p, miR-195-3p, miR-139-5p, and miR-31-5p expression [23, 24]. [score:5]
[1 to 20 of 1 sentences]
62
[+] score: 5
The expression of miR15a (4.19 fold) and miR-20b (3.42 fold) has been found to be higher in HPV -positive HNSCCs than in HPV -negative cases, while the expression of miR-139-3p (2.26 fold) and miR-145 (2.19 fold), among others, has been found to be lower in HPV -positive than in HPV -negative HNSCCs. [score:5]
[1 to 20 of 1 sentences]
63
[+] score: 5
To validate the identified phenotypes, the miRNAs that were down-regulated in clinical samples and Top-40 ranked in the phenotype screen (miR-150, miR-375, miR23b, miR-138, miR-139-5p and miR-9) were subjected to detailed functional analysis using HCT116, HT29, LS174T TR4, DLD1 TR7 and SW480 colon cancer cell lines. [score:4]
We have recently published a detailed functional analysis of miR-139-5p and hence miR-139-5p was not included in these analyses [25]. [score:1]
[1 to 20 of 2 sentences]
64
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
By 18 wks of E [2] treatment, the mammary glands were characterized by lobular involution and hyperplasia, and only 1 miRNA was down-regulated (miR-139) and 5 miRNAs were up-regulated (miR-20b, miR-21, miR-103, mir-107, miR-129-3p, and miR-148a). [score:5]
[1 to 20 of 1 sentences]
65
[+] score: 5
Prediction of functions of the best matched targets of each known miRNAs revealed that targets of some miRNAs were related to energy metabolism, including NADH dehydrogenase (miR-4144-3p, miR-1837, miR-125b*, and miR-36a*) and ATPase (miR-3666, miR-4115-5p, miR-4038-3p, miR-3668, miR-3559-3p, and miR-503); some of them were related to transcription initiation factor (miR-369-3p, miR-139, miR-4082-3p and miR-4148-5p), and splicing factor (miR-23a*, miR-767-3p, miR-463, miR-598 and miR-2881). [score:5]
[1 to 20 of 1 sentences]
66
[+] score: 5
Altered expressions of miR-1238-3p, miR-494, miR-6069, and miR-139-3p in the formation of chronic brucellosis. [score:3]
In one of our previous studies, more than 2,000 miRNAs were screened in peripheral blood mononuclear cells of patients with acute or chronic brucellosis, and we determined that while the expression level of miR-1238-3p increased, miR-494, miR-6069, and miR-139-3p decreased in the chronic group compared to the acute group. [score:2]
[1 to 20 of 2 sentences]
67
[+] score: 5
Blautia is also positively correlated with the expression level of miR-139, which is an miRNA with high expression levels in normal tissues. [score:5]
[1 to 20 of 1 sentences]
68
[+] score: 4
Moreover, miR-139-5p, miR-149, miR-449a and miR-342 were overexpressed in ER+ tumors with regard to TNBCs 10, 24, 48, 49. [score:3]
The “ECM & focal adhesion” node showed higher activity in ER-true tumors, and includes miR-139-5p, miR-149, miR-766, miR-342, miR-214* and miR-31. [score:1]
[1 to 20 of 2 sentences]
69
[+] score: 4
Moreover, the deletion c. *1934 delG at position 109594256 of Chr1 in Patient 3 (Table 6) disrupts not only the regulatory element GAIT but also the miR139-5p binding site, which is important for mRNA translational silencing of genes [55]. [score:4]
[1 to 20 of 1 sentences]
70
[+] score: 4
Previous microarray analyses revealed that 23 miRNAs are downregulated in CRC tissues (Additional file 1: Table S3), including miR-497 [21], miR-9 [22], miR-30a [23], and miR-139 [24]. [score:4]
[1 to 20 of 1 sentences]
71
[+] score: 4
All, except hsa-miR-139 and has-miR-375, were up-regulated in colon cancer tissues. [score:4]
[1 to 20 of 1 sentences]
72
[+] score: 4
Moreover, some differentially up-regulated microRNAs (such as miR-466h-5p, miR-135a-1*, miR-2137, miR-223, miR-139-5p, miR-29b-1*, and miR-7a) displayed earlier in PR8 infected lungs than in BJ501 infected lungs. [score:4]
[1 to 20 of 1 sentences]
73
[+] score: 4
Furthermore, we found 8 miRNAs (miR-95, miR-139, miR-379, miR-429, miR-509, miR-518e, miR-542-5p, and miR-659) downregulated in both 6 h aDCs and tDCs with respect to iDCs. [score:4]
[1 to 20 of 1 sentences]
74
[+] score: 4
The continuous downregulation observed in adenoma-carcinoma samples in case of miR-375, miR-378, miR-139-5p, miR-133a, and miR-422a was confirmed by others [36– 44]. [score:4]
[1 to 20 of 1 sentences]
75
[+] score: 4
p -value GO:0030834, Regulation of actin filament depolymerization SPTB, SPTBN1, SPTAN1, SPTA1, ADD1, EPB491.27 × 10 [−5] GO:0030837, Negative regulation of actin filament polymerization SPTB, SPTBN1, SPTAN1, SPTA1, ADD1, EPB492.71 × 10 [−5] GO:0002224, Toll-like receptor signaling pathway ATF2, CDK1, MEF2C, FOS, RELA, JUN, ATF1, NFKBIA2.96 × 10 [−5] GO:0008629, Induction of apoptosis by intracellular signals PML, BRCA1, YWHAB, TP53, BID, CDKN1A, RNF7, IFI163.52 × 10 [−5] GO:0043067, Regulation of programmed cell death SPRY2, TP53, ADAMTSL4, ETS1, TDGF1, RAF1, HOXA5, HOXA13, MSX1, MSX2, NKX2-5, CBL, INHBB, COL4A3, ACVR1C, TRAF21.92 × 10 [−5] GO:0007173, Epidermal growth factor receptor signaling pathway SPRY2, SPRY1, GRB2, PTPN11, TDGF1, RAF1, CBL9.44 × 10 [−5] MIMAT0000250(hsa-miR-139-5p) GO term Genes Adj. [score:4]
[1 to 20 of 1 sentences]
76
[+] score: 4
It has been demonstrated that FOXO1 expression is regulated by several microRNAs, such as miR-223, miR-182, miR-27a, miR-139 and miR-96 [39]– [43]. [score:4]
[1 to 20 of 1 sentences]
77
[+] score: 4
Other miRNAs from this paper: hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-133b
The following oligonucleotides were purchased from GenePharma (GenePharma, Shanghai, China): miR-133b mimics; miRNA negative control (designated as miR-NC); miR-139 mimic as a positive control; miR-133b antisense with a sequence complementary to the mature miR-133b; and miRNA antisense negative control (designated as inhibitor-NC), which is a negative control for miR-133b antisense. [score:3]
Once 70-80% confluent in 48-well plates, HEK-293T cells were cotransfected with 50 ng/well of each luciferase reporter plasmid and 10 nM/well of either miR-133b mimic, miR-139 mimic or miR-NC, as described above. [score:1]
[1 to 20 of 2 sentences]
78
[+] score: 3
In this follow up study, we selected nine miRNA candidates (miR-125-3p, miR-320c, miR-320d, miR-9-1, miR-139, miR-125a-5p, miR-4792, miR-376, miR-543, miRNA-381) for validation in the independently recruited patients with early-stage (I, II) colon cancer. [score:1]
MiR-9-1, miR-125a-3p, miR-125a-5p, miR-320c, miR-320d, miR-4792, miR-376, miR-139, miR-543, and miR-381(MS00010752, MS00008554, MS00003423, MS00041867, MS00031710, MS00045087, MS00007392, MS00003493, MS00010080, MS00004116, QIAGEN, Valencia, CA) were selected for downstream validation. [score:1]
Detection of miR-4792 and miR-139 significantly varied across technical triplicates possibly due to its high Ct value beyond 35. [score:1]
[1 to 20 of 3 sentences]
79
[+] score: 3
In studies examining responses to IL-1β, the processes of disrupted cartilage homeostasis have been found to be regulated by several miRNAs, including miR-145, miR-139, miR-9, miR-193b and miR-320 [20– 24]. [score:2]
An increasing number of studies have indicated that miRNAs participate in the pathogenesis of osteoarthritis, with confirmation for miR-139, miR-140, miR-23a-3p and miR-365 [6– 9]. [score:1]
[1 to 20 of 2 sentences]
80
[+] score: 3
L. Rask, E. Balslev, R. Søkilde, E. Høgdall, H. Flyger, J. Eriksen, T. Litman, Differential expression of miR-139, miR-486 and miR-21 in breast cancer patients sub-classified according to lymph node status. [score:3]
[1 to 20 of 1 sentences]
81
[+] score: 3
According to our results, we hypothesized that circRNA_001059 may act as an inhibitor of miRNA by binding several specific miRNAs, including miR-30c-1*, miR-30c-2*, miR-122*, miR-139-3p, miR-339-5p and miR-1912. [score:3]
[1 to 20 of 1 sentences]
82
[+] score: 3
MiRNA is also common in hepatocellular carcinoma, an example is that Au SL et al. ’s finding suggests that enhancer of zeste homolog 2 (EZH2) exerts its prometastatic function through epigenetic silencing of multiple tumor suppressor miRNAs including miR-101, miR-139-5p, let-7c, miR-125b, and miR-200b [18]. [score:3]
[1 to 20 of 1 sentences]
83
[+] score: 3
Moreover, we showed that both strands of pre- miR-139 (miR-139-5p and miR-139-3p) targeted matrix metalloprotease 11 in bladder cancer [23]. [score:3]
[1 to 20 of 1 sentences]
84
[+] score: 3
Oncogene 62 Schmitz KJ Helwig J Bertram S Sheu SY Suttorp AC 2011 Differential expression of microRNA-675, microRNA-139-3p and microRNA-335 in benign and malignant adrenocortical tumours. [score:3]
[1 to 20 of 1 sentences]
85
[+] score: 3
Other miRNAs from this paper: hsa-mir-28, hsa-mir-100, hsa-mir-518b
It has been shown that RAP1B is suppressed by miR-518b in ESCC and by miR-139 and miR-100 in CRC [19, 21, 23]. [score:3]
[1 to 20 of 1 sentences]
86
[+] score: 3
Other miRNAs such as miR-192, miR-139-5p, miR-483-5p, miR-142-3p, miR-142-5p, or miR-375 have not been previously described to be expressed in HSCs. [score:3]
[1 to 20 of 1 sentences]
87
[+] score: 3
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Note that the expression of ten of the 65 miRNAs we identified in the current study (miR-101, miR-127-3p, miR-139-5p, miR-142-5p, miR-185, miR-195, miR-218, miR-29a, miR-29c, miR-381) has been detected in samples of adult human hippocampus containing different subregions [34]. [score:3]
[1 to 20 of 1 sentences]
88
[+] score: 3
Several miRNAs, such as miR-101 [6], miR-122 [7], [8], [9] miR-373 [10], miR-221/222 [11], [12], [13], miR-195 [14], miR-30d [15], miR-125b [16], miR-18a [17], miR-139 [18], miR-223 [19] and miR-29 [20], have already been reported to regulate HCC tumor progression and metastasis by regulating key genes such as Mcl-1, ADAM17, YAP, DDIT4, Cyclin D1, CDK6, E2F3, Galphai2, LIN28B, estrogen receptor-α, Rho-kinase 2, Stathmin 1 and Bcl-2 and so on. [score:3]
[1 to 20 of 1 sentences]
89
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
[1 to 20 of 2 sentences]
90
[+] score: 2
Moreover, numerous miRNAs strongly dysregulated in tumor samples were absent from the sera (for example miR-205, miR-199a/b, and miR-139) (Tables 3 and 4). [score:2]
[1 to 20 of 1 sentences]
91
[+] score: 2
Moreover, 37 miRNAs were regulated by Sp110 in H37Ra-infected macrophages only (i. e., miR-106b, miR-1198, miR-139, miR-151, miR-25, miR-146a and miR-34c; Fig. 5c,). [score:2]
[1 to 20 of 1 sentences]
92
[+] score: 2
For example, microRNA-139-5p regulates the proliferation of hematopoietic progenitors and is repressed during BCR-ABL -mediated leukemogenesis [15]. [score:2]
[1 to 20 of 1 sentences]
93
[+] score: 2
At least 20 cellular miRNAs were differentially expressed in the six glioblastomas assayed here compared to non-tumor brain tissue, many of which (miR-128, miR-124, miR-7, miR-132, miR-139) are consistently dysregulated in not only gliomas but also other brain cancers including medulloblastomas and neuroblastomas [33]. [score:2]
[1 to 20 of 1 sentences]
94
[+] score: 2
Thirteen mRNA were specifically related to homozygous/heterozygous status of KIT mutation: miR-518f, miR-331, miR-628, miR-145, miR-139, miR-335, miR-526b, miR-190, miR-548c, miR-202, miR-339, miR-203, and miR-301b (Anova test p<0.05). [score:2]
[1 to 20 of 1 sentences]
95
[+] score: 2
Other miRNAs from this paper: hsa-mir-22, hsa-mir-375, hsa-mir-652
Four most strongly expressed miRNAs, miR-375, miR-652, miR-22, and miR139-5p, were selected for further validation by using individual TaqMan® microRNA assays. [score:2]
[1 to 20 of 1 sentences]
96
[+] score: 2
et al. 2007. miR-21, miR-23a, miR-210 and miR-139, miR-128, miR-181 are listed to show that the deep sequence data (NGS) are consistent with the pubilished results. [score:1]
The miR-21, miR-23a, miR-210 and miR-139, miR- 128 and miR-181 are listed as controls to shown that the deep sequence data (NGS) are consistent with the published results [27, 35– 39]. [score:1]
[1 to 20 of 2 sentences]
97
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-100, hsa-mir-106a, hsa-mir-107, hsa-mir-192, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-182, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-221, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-134, hsa-mir-146a, hsa-mir-149, hsa-mir-150, hsa-mir-154, hsa-mir-320a, hsa-mir-155, hsa-mir-128-2, hsa-mir-200a, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-302c, hsa-mir-367, hsa-mir-370, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-379, hsa-mir-328, hsa-mir-151a, hsa-mir-135b, hsa-mir-335, hsa-mir-133b, hsa-mir-449a, hsa-mir-451a, hsa-mir-410, hsa-mir-486-1, hsa-mir-146b, hsa-mir-520f, hsa-mir-518d, hsa-mir-517c, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-584, hsa-mir-602, hsa-mir-629, hsa-mir-638, hsa-mir-449b, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-298, hsa-mir-1246, hsa-mir-1908, hsa-mir-718, hsa-mir-2861, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-4728, hsa-mir-4734, hsa-mir-378j, hsa-mir-6165, hsa-mir-486-2
Ruiz-Martinez et al. (2016) MiR-378a, MiR-379, MiR-139- 5p, MiR-200b-5p, MiR-151a-5p, MiR-30a-3p, MiR-200b-5p, MiR-629, MiR-100, and MiR-154-3p30 blood plasma samples (10 patients affected by lung adenocarcinomas, 10 with lung granulomas, and 10 healthy smokers) qRT-PCR analysis The production of exosomes containing miRNAs in the lung carcinoma cells are completely different to those present in healthy control cells from which neoplastic cells originated. [score:1]
[1 to 20 of 1 sentences]
98
[+] score: 1
org/), a set of miRNAs were predicted to have potential interaction with circUBAP2, including miR-150, miR-135, miR-101, miR-181, miR-23, miR-149, miR-139, miR-491, miR-124, miR-301m miR-328, miR-122, miR-186, let-7, miR-132, miR-191, miR-425, miR-125, miR-149, miR-143, and miR-146a. [score:1]
[1 to 20 of 1 sentences]
99
[+] score: 1
66 hsa-miR-511 −4.05 16.61 hsa-miR-26b −4.01 16.15 hsa-miR-210 −4.01 16.15 hsa-miR-489 −3.98 15.78 hsa-miR-22* −3.98 15.74 hsa-miR-15a* −3.97 15.70 hsa-miR-106a −3.92 15.15 hsa-miR-331-5p −3.91 15.04 hsa-miR-194 −3.88 14.73 hsa-miR-139-5p −3.85 14.38 hsa-miR-193a-5p −3.84 14.37 hsa-miR-29a −3.80 13.94 hsa-miR-24 −3.75 13.43 hsa-miR-140-5p −3.71 13.12 hsa-miR-28-3p −3.69 12.91 hsa-miR-151-3p −3.67 12. [score:1]
[1 to 20 of 1 sentences]
100
[+] score: 1
We chose the best predictions for each SNP: for rs1047383, hsa-miR-124-1, hsa-miR-139, hsa-miR-140, hsa-miR-144, hsa-miR-377, hsa-miR-506, has-miR-548h, hsa-miR-1324 and hsa-mir-3148; and for rs708910, hsa-miR-582 and hsa-miR-140. [score:1]
[1 to 20 of 1 sentences]