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38 publications mentioning hsa-mir-885

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-885. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 330
To further validate that β-catenin serves as miR-885-5p binding target, it was determined whether or not miR-885-5p -mediated suppression of β-catenin expression indeed suppressed β-catenin transcriptional activity. [score:9]
In fact, upregulation of miR-885-5p inhibited the Wnt/β-catenin signaling pathway and expression of some of its downstream genes (Figures 5– 7). [score:8]
These data demonstrate that miR-885-5p inhibited the expression of β-catenin by directly targeting its 3′-UTR. [score:8]
In this study, we also found miR-885-5p in HCC inhibited the expression of β-catenin leads to suppression of the Wnt/β-catenin signaling pathway. [score:7]
Expression of miR-885-5p is downregulated in highly malignant HCC tissues and cell lines. [score:6]
In this study, consistent with in vitro results, our animal mo del experiments show that upregulation of miR-885-5p also inhibits metastasis of HCC (Figure 4). [score:6]
Downregulated expression of miR-885-5p in highly malignant HCC tissues and cell Lines. [score:6]
Conversely, downregulation of miR-885-5p increased the activity of its Wnt/β-catenin signaling pathway and expression of its downstream genes (Supplementary Figure S3). [score:6]
miR-885-5p may suppress the form of destruction complex indirectly, and this suppression results in absence of β-catenin in nuleus; however, this mechanism will be further studied. [score:6]
In fact, we observed that upon miR-885-5p down-regulation, proliferation of HepG2 cells increased, suggesting that miR-885-5p also suppressed HCC growth in vitro. [score:6]
To verify the predicted target, we performed dual-luciferase reporter assays, which indicated that co -expression of miR-885-5p mimics in HCCLM3 cells significantly inhibited the activity of luciferase which contained the wild-type, but not the mutant, 3′-UTR of CTNNB1 (Figure 5B). [score:6]
Yan et al. showed that miR-885-5p inhibited the expression of MMP9 indirectly. [score:6]
To determine whether miR-885-5p is differentially expressed in the HCC tissues of different TNM stages of tumor development, the relationship between expression of miR-885-5p and clinicopathology was analyzed by either the χ [2] method or Fisher's exact test. [score:6]
Conversely, β-catenin protein level was upregulated by the infection of lv-miR-885-locker which caused knockdown of miR-885-5p in HepG2 cells (Supplementary Figure S3A). [score:5]
Overexpression of miR-885-5p inhibits proliferation of HCCLM3 cells in vivo and prolongs the survival of tumor-bearing Mice. [score:5]
miR-885-5p inhibits HCC metastasis and growth in vitro and in vivoTo better understand the biological functions of miR-885-5p in the progression of HCC, we overexpressed miR-885-5p in HCC cell lines, HCCLM3 and SK-Hep-1, which have high metastatic and malignant properties. [score:5]
Figure 3Overexpression of miR-885-5p in HCCLM3 and SK-Hep-1 reduced the migratory and invasive potential in vitro(A) miR-885-5p expression levels after treatment of HCC cell lines with either miR-885-5p mimics or miR-NC (negative control). [score:5]
The invasiveness of miR-885-5p -expressing HCCLM3 and SK-Hep-1 cells was downregulated as demonstrated by transwell assays with Matrigel. [score:5]
Figure 4Overexpression of miR-885-5p inhibits proliferation of HCCLM3 cells in vivo and prolongs the survival of tumor-bearing Mice(A– D) HCCLM3-lv- miR-885-5p or HCCLM3-lv-NC tumor-bearing mice were euthanized after 43 days, and the lungs were histologically examined for metastatic foci. [score:5]
In fact, intratumoral injection of cholesterol-conjugated miR-885-5p mimics demonstrated that when miR-885-5p expression in SK-Hep-1 cells was elevated (Supplementary Figure S2A), whereas the tumor growth was inhibited (Supplementary Figure S2C and S2D). [score:5]
The results showed that the protein levels of CTNNB1 in HCC tissues with weak miR-885-5p expression were significantly higher than those in HCC tissues with strong miR-885-5p expression (Figure 8). [score:5]
Lentiviral -mediated overexpression or inhibition of miR-885-5p. [score:5]
Taken together, these data are likely to indicate that miR-885-5p is a potential biomarker for the diagnosis of HCC as well as a therapy target for the development of novel therapies to treat HCC. [score:4]
β-catenin is the direct target of miR-885-5p. [score:4]
miR-885-5p regulates the Wnt/β-catenin pathway by targeting CTNNB1. [score:4]
miR-885-5p downregulates β-catenin. [score:4]
We showed that ectopic miR-885-5p downregulated the activity of Wnt/β-catenin signaling pathway. [score:4]
Figure 7miR-885-5p regulates the Wnt/β-catenin pathway by targeting CTNNB1(A), analysis of β-catenin in the cytoplasmic and nuclear fractions from HCCLM3 or SK-Hep-1 cells transfected with the miR-885-5p mimics or NC. [score:4]
These data suggest that miR-885-5p levels were downregulated during the progression of HCC metastasis. [score:4]
miR-885-5p was found to be downregulated in neuroblastomas and to bind 3′UTR of CDK2 and MCM5 [30]. [score:4]
In an effort to further investigate whether the deregulated expression of miR-885-5p correlates with the survival of HCC patients, the expression levels of miR-885-5p were determined in 51 HCC samples from 51 individual HCC patients (Figure 2A and 2B). [score:4]
Low miR-885-5p expression correlates with poor survival of HCC patients. [score:3]
Afanasyeva1 et al. reported that miR-885-5p binds CDK2 and MCM5, activates p53 and inhibits proliferation and survival. [score:3]
To determine the relationship between miR-885-5p and expression of β-catenin in human HCC tissues, immunohistochemical analyses were conducted in the same HCC tissue microarrays as those used in miR-885-5p in situ hybridization with β-catenin antibody. [score:3]
The miR-885-5p lentiviral expression vector, the miR-885-5p-locker vector and the packaging vectors, plv-PACK-1, plv-PACK-2 and plv-PACK-1, were purchased from Biostettia Biotechnology (San Diego, CA). [score:3]
Therefore, these results confirm that miR-885-5p decreased the activity of the Wnt/β-catenin signaling pathway, possibly leading to the suppression of HCC metastasis. [score:3]
To better understand the biological functions of miR-885-5p in the progression of HCC, we overexpressed miR-885-5p in HCC cell lines, HCCLM3 and SK-Hep-1, which have high metastatic and malignant properties. [score:3]
The significance was determined by a x [2] test as shown in Table 1 and Table 2. The correlation between miR-885-5p expression and patient survival was determined by the Kaplan–Meier method. [score:3]
Overexpression of miR-885-5p in HCCLM3 and SK-Hep-1 reduced the migratory and invasive potential in vitro. [score:3]
Based on our results, we propose that miR-885-5p inhibits metastasis of HCC. [score:3]
Most HCC tissues expressed different levels of miR-885-5p (Figure 1A). [score:3]
There was no significant relationship between miR-885-5p expression and other clinicopathological factors, such as histological grade, gender and age (P > 0.05; Table 1). [score:3]
In contrast, the results of our study provided strong evidence that miR-885-5p, through binding CTNNB1, inhibited metastasis and growth of HCC. [score:3]
Correlation between miR-885-5p expression and pathological grading of HCC. [score:3]
Since it was previously reported that miR-885-5p can inhibit proliferation of neuroblastoma [30], we used HepG2 cells to assess whether miR-885-5p could also decrease the proliferation of these cells (Supplementary Figure S1A and S1B). [score:3]
The expression trend of β-catenin was conversely with miR-885-5p (Figure 8) (Table 2). [score:3]
The liver tissue microarrays for determining miR-885-5p expression were purchased from Chaoying Biotechnology (Xi'an, China). [score:3]
miR-885-5p expression correlated inversely with β-catenin. [score:3]
In addition, we determined that miR-885-5p suppressed metastasis of HCC in vitro and in vivo. [score:3]
Plots represent the percentage of tissue samples with different expression level of β-catenin (y-axis) in each group that was defined as miR-885-5p negative, weak, moderate or strong (x-axis). [score:3]
miR-885-5p suppresses the Wnt/β-catenin signaling pathway. [score:3]
Previous studies reported that miR-885-5p suppresses tumor cell proliferation and survival of neuroblastoma [30] as well as metastasis of glioblastomas [29]. [score:3]
Here, we demonstrate that miR-885-5p functions an anti-metastatic miRNA and a negative regulator of the Wnt/β-catenin signaling pathway, which is a key pathway in the development and progression of HCC and various other tumors. [score:3]
We found that the expression of miR-885-5p negatively correlates with the invasive and metastatic potential of different HCC patient's tissues and cell lines. [score:3]
We confirmed that this technique could effectively overexpress miR-885-5p in tumors of an HCC mouse mo del. [score:3]
Together, these results indicate that miR-885-5p significantly inhibited HCC cell migration and invasion in vitro. [score:3]
Here, we found that control HCCLM3 cells and SK-Hep-1 cells exhibited both cytoplasmic and nuclear localization of β-catenin, whereas in the miR-885-5p -overexpressing cells, β-catenin was associated with cell-cell junctions (Figure 6). [score:3]
Our in vitro and in vivo results provided evidences that miR-885-5p functioned as a suppressor of HCC. [score:3]
Patients in stage II (n = 81) exhibited higher expression of miR-885-5p than those in stage III (n = 146; P < 0.001). [score:3]
Our analyses revealed that miR-885-5p expression was a predictor of survival of HCC patients (Figure 2). [score:3]
We further explored the pathophysiological functions of miR-885-5p and found that expression of miR-885-5p in the highly metastatic HCC cell lines decreased the migration and invasiveness of the cells in vitro (Figure 3). [score:3]
Expression of miR-885-5p correlates with survival of HCC patients. [score:3]
Expression of miR-885-5p in HCC was performed by in situ hybridization tissue arrays that contained 227 cores of HCC tissue from 227 patients. [score:3]
This result indicates that miR-885-5p inhibited not only the metastatic progression of HCC but also the growth of HCC. [score:3]
We explored the possible molecular mechanism underlying the functions of miR-885-5p in HCC is that CTNNB1 is a novel target gene of miR-885-5p. [score:3]
miR-885-5p inhibits HCC metastasis and growth in vitro and in vivo. [score:3]
Figure 2(A) Moderate expression of miR-885-5p in HCC tissues. [score:3]
Subsequently, Yan et al. reported that miR-885-5p reduced MMP-9 expression, which mediates the invasion of glioblastomas [29]. [score:3]
Together, such results suggest that miR-885-5p should be considered a potential target for HCC gene therapy. [score:2]
Furthermore, in cytoplasmic fraction prepared from the miR-885-5p -overexpressing HCCLM3 cells, the amount of β-catenin was decreased; therefore, a lesser amount of β-catenin accumulated in the nucleus of these cells as compared to control cells (Figure 7A). [score:2]
Moreover, both number and size of metastatic nodules in the lung were significantly decreased in the miR-885-5p overexpression group compared to the vector group after HCCLM3 cells in situ were grown for 43 days (Figure 4D). [score:2]
These observations suggest that miR-885-5p may be a negative regulator of metastasis in HCC. [score:2]
Knockdown of miR-885-5p in nonmetastatic HepG2 cells indicated that lv-miR-885-5p-locker-infected HepG2 cells possess an increased ability to grow (Supplementary Figure S1). [score:2]
Wound healing assay demonstrated that miR-885-5p suppressed cell migration in HCCLM3 and SK-Hep-1 cells (Figure 3B). [score:2]
Additionally, the mutant3′-UTR of CTNNB1 with site-specific mutations in the response element of miR-885-5p was created by site-directed mutagenesis using the primers CTNNB1-MUT-F: 5′-TTTTTTTTAAGAATATCTGATTACGTACTGACTTT CTTGCTTT-3′ and CTNNB1- MUT-R: 5′-AAAGCAAGAA AGTCAGTACGTAATCAGATATTCTTAAAAAAAA-3′. [score:2]
Taken together, these results strongly suggest that miR-885-5p acted as a negative regulator of metastatic progression of HCC. [score:2]
In fact, miR-885-5p was first identified from a pheochromocytoma in 2010 [27], and we previously reported that circulating miR-885-5p is present at higher levels in patients with cirrhosis or HCC than in healthy, control individuals [28]. [score:1]
We found that repeated intratumor injections of miR-885-5p agomirs can actually halt HCC growth. [score:1]
To identify the protecting function, we determined whether miR-885-5p levels correlate with the survival of HCC patients. [score:1]
Either HCCLM3/lv-miR-885-5p or HCCLM3/lv-NC cells (5 × 10 [6]) were injected subcutaneously (S. C. ) into the upper left flank region of 12 NOD/SCID mice. [score:1]
The transwell assays without Matrigel clearly indicated that miR-885-5p clearly suppresses migration of HCCLM3 and SK-Hep-1 cells when compared to control groups (Figure 3C and 3D). [score:1]
Next, orthotopic liver implantation of HCCLM3/lv-miR-885-5p and HCCLM3/lv-NC cells into NOD/SCID mice was performed. [score:1]
Levels of miR-885-5p were decreased in higher metastatic HCC cell lines (Figure 1B). [score:1]
The result showed miR-885-5p restoration significantly repressed the growth of the HCCLM3 cells (Figure 4C). [score:1]
Additionally, β-catenin protein levels were decreased by transfection of the miR-885-5p mimics into HCCLM3 or SK-Hep-1 cells (Figure 5D). [score:1]
Furthermore, we examined the role of miR-885-5p in the mobility and invasiveness of HCC cells using transwell chambers with or without Matrigel. [score:1]
Kaplan-Meier survival analyses showed that the higher miR-885-5p levels in the HCC tissues significantly correlated with the markedly prolonged overall survival of these HCC patients (Figure 2C). [score:1]
Immunofluorescence staining of in HCCLM3 (A) or SK-Hep-1 (B) cells transfected with miR-885-5p mimics or NC demonstrates differential localization. [score:1]
Cytoplasmic miR-885-5p are denoted by red arrowheads, and nucleus are denoted by blue arrowheads. [score:1]
Furthermore, CTNNB1 mRNA levels were found to be decreased by transfection of the miR-885-5p mimics into HCCLM3 or SK-Hep-1 cells (Figure 5C). [score:1]
The cells were seeded onto six-well culture plates and transfected the next day, cells were transfected with 50 nM miR-885-5p mimics or negative control microRNAs (miR-NC). [score:1]
The miR-885-5p mimics and the negative controls were purchased from Applied Biosystems (Carlsbad, CA). [score:1]
Establishment of an additional set of orthotopic HCCLM3 tumors and found that miR-885-5p also prolonged the survival of the tumor-bearing mice (Figure 4E). [score:1]
The miR-885-5p mimics were purchased from Ambion (Foster City, CA). [score:1]
Figure 6Immunofluorescence staining of in HCCLM3 (A) or SK-Hep-1 (B) cells transfected with miR-885-5p mimics or NC demonstrates differential localization. [score:1]
Additionally, this phenotype led us to further study the biological effects of miR-885-5p. [score:1]
The cholesterol-conjugated miR-885-5p mimics and the respective negative controls for in vivo RNA delivery were obtained from Ribobio Co. [score:1]
In addition, we found that miR-885-5p significantly decreased the levels of the proteins, MYC, VEGF, pro-MMP7, and Survivin (Figure 7C and Supplementary Figure S3C), which are downstream proteins of Wnt/β-catenin signaling pathway. [score:1]
Firstly, two Luciferase-labeled stable cell lines were established, HCCLM3/lv-miR-885-5p and HCCLM3/lv-NC (Figure 4A and 4B). [score:1]
Immunofluorescence staining of β-catenin in HCC cell lines transfected with miR-885-5p. [score:1]
Figure 1(A) In situ hybridization of miR-885-5p in 227 cores HCC tissue array, including 81 T2N0M0 staged HCC tissues and 146 T3N0M0 staged HCC tissues. [score:1]
Our study provides in vitro and in vivo evidence to support a rationale for developing miR-885-5p as a therapeutic agent to treat HCC-related metastasis. [score:1]
Our study shows that the lower miR-885-5p levels or higher β-catenin levels in the HCC tissues significantly correlated with poorer overall survival of the HCC patients. [score:1]
Figure 5(A), Alignment of miR-885-5p with CTNNB1 at the 3′-UTR. [score:1]
Notably, in our study HCC tissues and cell lines with higher metastatic properties display lower levels of miR-885-5p than less metastatic tissues and cell lines (Figure 1). [score:1]
Recently, miR-885-5p was reported as a diagnosis and prognosis factor in plasma or whole blood in detection of pancreatic cancer [31, 32]. [score:1]
In situ detection of miR-885-5p in the patient HCC and healthy control samples was performed on a paraffin-embedded tissue microarray using a miRCURY LNA™ microRNA in situ hybridization (ISH) Optimization Kit for formalin-fixed, paraffin-embedded samples (Exiqon) according to the manufacturer's instructions. [score:1]
Levels of miR-885-5p were 1,000-fold higher in cells after transfection with the miR-885-5p mimics than those transfected with the control miRNA (Figure 3A). [score:1]
Although the function of miR-885-5p has been studied in vitro in a few cancer cell lines; however, the functions and mechanisms of miR-885-5p in the progression of HCC remain yet unclear. [score:1]
In situ hybridization In situ detection of miR-885-5p in the patient HCC and healthy control samples was performed on a paraffin-embedded tissue microarray using a miRCURY LNA™ microRNA in situ hybridization (ISH) Optimization Kit for formalin-fixed, paraffin-embedded samples (Exiqon) according to the manufacturer's instructions. [score:1]
The miR-885-5p mimics (50 nM/well; Applied Biosystems, CA) were co -transfected with 100 ng/well luciferase reporter plasmids and 2 ng/well plasmid pRL-TK. [score:1]
The findings suggest that miR-885-5p may be a biomarker for HCC prognosis. [score:1]
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2
[+] score: 80
Further RT-qPCR confirmed that miR-885-5p over expression leads to down-regulated expression of Wnt5 mRNA level (Fig. 7A ). [score:8]
Our results suggest that miR-885-5p functions as a negative regulator of osteogenic differentiation of BSMCs by repressing Runx2 and thereby inhibiting expression of osteoblast-related genes. [score:6]
Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were predicted to participate in Wnt signaling pathway through regulating their potential gene targets. [score:6]
0114627.g005 Figure 5 Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were predicted to participate in Wnt signaling pathway through regulating their potential gene targets. [score:6]
0114627.g004 Figure 4 Three under-expressed miRNAs (miR-203, miR-885-5p, and miR-320c) were predicted to participate in RNA transport pathway through regulating their potential gene targets. [score:6]
Three under-expressed miRNAs (miR-203, miR-885-5p, and miR-320c) were predicted to participate in RNA transport pathway through regulating their potential gene targets. [score:6]
0114627.g002 Figure 2. TaqMan real-time RT-PCR to validate the expression levels of nine up regulated miRNAs, including let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b (A) and three down regulated miRNAs, including miR-885-5p, miR-181a, and miR-320c (B) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 7 days. [score:5]
To determine whether exosomal miR-885-5p are linked to BMP2 -induced BSMCs osteogenic differentiation through their targets, BSMCs were treated with BMP2 for 24 and 48 h after expressing miR-885-5p for 12 h. As expected, Runx2 protein level was enhanced by BMP2 in cells transfected with miR-Control (Fig. 7B ). [score:5]
TaqMan real-time RT-PCR to validate the expression levels of nine up regulated miRNAs, including let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b (A) and three down regulated miRNAs, including miR-885-5p, miR-181a, and miR-320c (B) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 7 days. [score:5]
RT-qPCR to detect the expression of Wnt5 mRNA level when miR-885-5p over expression. [score:5]
0114627.g003 Figure 3 Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were selected as examples for examining miRNA-mRNA relationships in RNA degradation. [score:3]
Nine up regulated miRNAs (let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b) and five down regulated miRNAs (miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 7 days. [score:3]
Western Blot to detect Runx2 protein level in BSMCs were treated with BMP2 for 24 and 48 h after expressing miR-885-5p and miR-Control for 24, 48 h. Data shown are representative of three independent experiments. [score:3]
However, miR-885-5p expression restrained the increase of Runx2 protein after BMP2 treatment (Fig. 7B ). [score:3]
While miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c were significantly under expressed in individual exosomal samples along with the time course at 0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 7 days (Fig. 2 ). [score:3]
While miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c were significantly under expressed in individual exosomal samples. [score:3]
nine up regulated miRNAs (let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b) and five down regulated miRNAs (miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c) from miRNA array were further quantitated by TaqMan miRNA assays (Applied Biosystems). [score:2]
miR-885-5p regulates BMP2 -induced osteogenic differentiation. [score:2]
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3
[+] score: 45
Yan et al. showed that miR-885-5p inhibited the expression of MMP9 indirectly [64]. [score:6]
The target genes of these miRNAs and the immunologically effective pathways that are potentially manipulated by these miRNAs are presented in Figs 2– 4. According to these analyses, miR-885-5p is involved in the regulation of 3085 gene expressions. [score:6]
One of the 28 miRNAs in which the expression was upregulated in chronic brucellosis is miR-885-5p. [score:6]
One increased miRNA (miR-885-5p) that targets genes of immunologically effective pathways is shown in Fig 2. Other increased miRNAs (miR-483-3p and miR-328) that target genes of immunologically effective pathways are shown in Figs 3 and 4, respectively. [score:5]
They provided evidence that CDK2, which participates in cell cycle regulation and is especially critical during the G1 to S phase transition, and MCM5, which is involved in the initiation of DNA replication, are direct miR-885-5p targets [63]. [score:5]
The predicted target genes of miRNAs that uniquely expressed in the chronic cases, including miR-885-5p, miR-483-3p, and miR-328, were analysed. [score:5]
They demonstrated that miR-885-5p downregulates cyclin -dependent kinase (CDK2) and that the mini-chromosome maintenance protein (MCM5) activates p53. [score:4]
Afanasyeva et al. show that miR-885-5p inhibits cell proliferation and survival and promotes cellular senescence and apoptosis. [score:3]
According to KEGG pathways analysis, miR-885-5p was linked to the MAPK signalling pathway, regulation of the actin cytoskeleton, ubiquitin -mediated proteolysis, endocytosis, focal adhesion, cytokine-cytokine receptor interactions, protein processing in the endoplasmic reticulum, the JAK-STAT signalling pathway, the cell cycle, tight junction, the chemokine signalling pathway, and leukocyte transendothelial migration pathways in chronic brucellosis. [score:2]
Approximately 3,085 genes were regulated by miR-885-5p. [score:2]
Pathway analysis of miR-885-5p according to KEGG function annotations. [score:1]
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[+] score: 25
However, miR-885-5p was not translatable across species and did not change. [score:3]
The largest fold increase miRNAs (miR-122-5p and miR-885-5p) were highly correlated across patients in the training set (Fig. 3A). [score:1]
Cisplatin had no effect on miR-122-5p, miR-885-5p, miR-151a-3p or miR-382-5p (Fig. 5E–H). [score:1]
miR-885-5p remained elevated longer than miR-122-5p (Fig. 6B). [score:1]
Figure (A) Pearson correlation plot of circulating miR-885-5p and miR-122-5p across APAP-TOX and APAP-no TOX patients. [score:1]
miR-122-5p, miR-885-5p, miR-151-3p and miR-382-5p reported acute liver injury due to causes other than acetaminophen, which is consistent with them being liver specific and demonstrates that this panel has utility in the diagnosis of acute liver injury due to multiple causes. [score:1]
Figure (E– H) present miR-122-5p, miR-885-5p, miR-151a-3p and miR-382-5p in control mice, APAP overdose mice and cisplatin -induced acute kidney injury (AKI) mice. [score:1]
However, the data presented in this study clearly demonstrate that miR-885-5p does not increase with acetaminophen toxicity in mice, an important limitation. [score:1]
However, there was no difference in miR-122-5p, miR-885-5p, miR-151a-3p or miR-382-5p (Table 1). [score:1]
The 3 largest fold increase miRNAs (miR-122-5p, miR-885-5p and miR-151a-3p) and the miRNA with the lowest prediction error from the classifier mo del (miR-382-5p) were taken forward and tested for specificity and sensitivity. [score:1]
miR-885-5p, miR-151a-5p and miR-382-5p were inferior to ALT for early prediction of liver injury (Fig. 7). [score:1]
The largest fold change miRNAs (miR-122-5p, miR-885-5p and miR-151-3p) and the best discriminating miRNA (miR-382-5p) were taken forward and tested for specificity. [score:1]
The largest median (IQR) increased circulating miRNAs were miR-122-5p 68 (11–277), miR-885-5p 57 (17–372) and miR-151a-3p 57 (16–360) (Fig. 2B). [score:1]
Ago2-bound miR-885-5p also increases with injury and both these miRNAs were localised to hepatocytes by in situ hybridization on human liver explants removed at transplantation for acetaminophen toxicity. [score:1]
The most abundant miRNA species in the liver 20, miR-122-5p, was the highest increased circulating miRNA but other species were elevated to comparable degrees (miR-885-5p, miR-151-3p) or were ranked higher by random forest analysis in terms of ability to report injury (miR-382-5p). [score:1]
After antibody -mediated pull down of Ago2 (corrected by IgG control), acetaminophen toxicity induced a significant increase in the amount of miR-122-5p and miR-885-5p specifically bound to Ago2 (Fig. 3B,C), consistent with both miRNAs being released bound to this protein. [score:1]
miR-122-5p and miR-885-5p are released from human hepatocytes bound to the carrier protein Ago2. [score:1]
In situ hybridization for miR-122-5p and miR-885-5p was performed on liver explants removed following acetaminophen overdose. [score:1]
Comparative biomarker profiles for miR-122-5p, miR-885-5p, miR-151-3p and miR-382-5p are summarized in supplementary Table 5. Although miR-122-5p had the highest fold increase in APAP-TOX patients, it was ranked 11th place in the miRNA panel, suggesting that other microRNA species may have greater clinical utility. [score:1]
Figure (B– D) represent the relative Ago2 fraction for miR-122-5p, miR-885-5p and miR-151a-5p respectively in APAP-TOX (N = 6) and APAP-no TOX (N = 6) patients. [score:1]
Figure (A– D) present circulating miR-122-5p, miR-885-5p, miR-151a-3p and miR-382-5p in APAP-no TOX patients and patients with acute liver injury (ALI) induced by APAP overdose or another aetiology (non-APAP). [score:1]
Images from hematoxylin and eosin (H&E) and in situ hybridization for miR-122-5p and miR-885-5p are presented. [score:1]
These data suggest release of miR-122 and miR-885 from the same cells attached to the same carrier protein. [score:1]
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5
[+] score: 18
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-21, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-28, hsa-mir-30a, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30d, hsa-mir-34a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-194-1, hsa-mir-194-2, hsa-mir-200a, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-196b, hsa-mir-484, hsa-mir-486-1, hsa-mir-1271, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-27a, bta-mir-30d, bta-mir-484, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-98, bta-mir-148b, bta-mir-200a, bta-mir-30a, bta-let-7a-1, bta-mir-342, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, bta-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-143, bta-mir-152, bta-mir-16a, bta-mir-194-2, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-199a-2, bta-mir-26a-1, bta-mir-28, bta-mir-335, bta-mir-338, bta-mir-378-1, bta-mir-486, bta-mir-885, bta-mir-96, bta-mir-1271, bta-mir-2299, bta-mir-199c, bta-mir-1388, bta-mir-194-1, bta-mir-378-2, hsa-mir-378b, bta-mir-3431, hsa-mir-378c, hsa-mir-4286, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, bta-mir-4286-1, bta-mir-4286-2, hsa-mir-378j, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, bta-mir-378d, bta-mir-194b, bta-mir-194b-2
Our analysis indicates that, about 3594 genes could be targeted by the eleven up-regulated miRNAs (bta-199a-3p, miR-98, miR-378, miR-21-5p, miR-148b, miR-4286, miR-885, miR-196a, miR-23b-3p, bta-miR-199c and miR-3431) whereas 1163 genes could be targeted by the three down-regulated miRNAs (bta-miR-335, miR-200a and bta-miR-2299-5p) in linseed oil -treated cows. [score:11]
Out of this number, 11 were up-regulated (bta-miR-4286, miR-885, miR-199c, miR-199a-3p, miR-3431, miR-98, miR-196a, miR-378, miR-23b-3p, miR-148b and miR-21-5p) while only 3 were down-regulated (miR-200a, miR-335 and miR-2299-5p) (Table  2). [score:7]
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6
[+] score: 16
The most upregulated miRNAs in hTERT-immortalized keratinocyte clones were less-studied miR-627-5p and miR-885-5p, although miR-885-5p has been reported to act as the post-transcriptional regulator of CASP3 expression which has anti-apoptotic and carcinogenic effects [44]. [score:7]
Inverse patterns of expression regulation of miR-34c-3p and miR-885-5p were found in the mo del system and clinical samples. [score:4]
MiR-335-5p, miR-579-3p, and miR-126-5p were shared by the expression profiles of HPV -positive tonsillar tumors and of the HPV immortalized keratinocyte clones, whereas miR-328-3p, miR-34c-3p, and miR-885-5p were shared by the miRNA profiles of HPV -negative tonsillar tumors and the HPV -negative keratinocytes. [score:3]
NT [b] Fold change Fold change hsa-miR-328-3p mir-328 −22.020 −2.806 hsa-miR-34c-5p mir-34 −16.419 4.851 hsa-miR-885-5p mir-885 48.377 −3.725 [a] tHFK HPV-immortalized human foreskin keratinocyte clones, pHFK primary human foreskin keratinocyte clones, iHFK hTERT-immortalized human keratinocyte clones [b] TT+ HPV -positive tonsillar tumors, TT- HPV -negative tonsillar tumors In the groups of HPV -positive tonsillar tumors and HPV-immortalized keratinocyte clones, we also evaluated the influence of HPV status on the changes in the miRNA expression profile. [score:1]
NT [b] Fold change Fold change hsa-miR-328-3p mir-328 −22.020 −2.806 hsa-miR-34c-5p mir-34 −16.419 4.851 hsa-miR-885-5p mir-885 48.377 −3.725 [a] tHFK HPV-immortalized human foreskin keratinocyte clones, pHFK primary human foreskin keratinocyte clones, iHFK hTERT-immortalized human keratinocyte clones [b] TT+ HPV -positive tonsillar tumors, TT- HPV -negative tonsillar tumors In the groups of HPV -positive tonsillar tumors and HPV-immortalized keratinocyte clones, we also evaluated the influence of HPV status on the changes in the miRNA expression profile. [score:1]
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7
[+] score: 13
miR-885-5p was one of the three downregulated miRNAs in glomeruli of DSA+. [score:4]
Whereas miR-30d suppresses TP53 [55], miR-885 activates it [56]. [score:3]
Based on inspection of the volcano plots and an in silico analysis of regulated pathways with DIANA miRPath v. 2.0 [10] we chose a set of 16 miRNAs for confirmation in microdissected glomeruli from patients with only HLA-class I DSAs: miR-let-7c, miR-28-3p, miR-29b, miR-30d, miR-99b, miR-125a-5p, miR-133a, miR-138, miR-146b, miR-195, miR-374b-3p, miR-484, miR-501-3p, miR-520e, miR-625-3p, miR-885-5p (Table  1). [score:2]
0.32; 0.19; 0.61; p = 0.018) and miR-885-5p (8.88e-6; 3.16e-7; 0.21e-4 vs. [score:1]
Glomerular miR-let-7c-5p (a), miR-28-3p (b), miR-30d-5p (d), miR-99b-5p (e), miR-125a-5p (f) and miR-195-5p (j), miR-374b-3p (k), miR-484 (l), miR-501-3p (m), miR-520e (n) and miR-885-5p (p) were higher in DSA+ than to controls. [score:1]
Glomerular miR-29b-3p (c) and miR-885-5p (p) were lower in DSA+ than in controls. [score:1]
2.87; 1.164; 7.76; p = 0.045) and miR-885-5p (6.56e-5; 9.83e-7; 4.04e-4 vs. [score:1]
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8
[+] score: 11
miR-885-5p is upregulated in head and neck cancer and oncocytic follicular carcinomas and acts by targeting caspase 3 [37]. [score:6]
miR-885-5p also targets CDK2 and MCM5, activates p53 and inhibits proliferation and survival in neuroblastoma [38]. [score:5]
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9
[+] score: 9
Five of these microRNAs could be validated in a second cohort, in which four of them were downregulated (let-7i, miR-10b, miR-221, and miR-320a) and one was upregulated (miR-885-5p) in liver metastases compared with the primary tumour. [score:6]
Furthermore, high serum miR-885-5p expression independently predicted prognosis (HR=2.9, 95% CI=1.1–7.5, P=0.0323), lymph node metastases (OR=3.0, 95% CI=1.3–7.2, P=0.0116) and distant metastases (OR=3.1, 95% CI=1.0–10.0, P=0.0456; Hur et al, 2015). [score:3]
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10
[+] score: 8
Remarkably, 10 of the 16 shared miRNAs were inversely regulated in T2DM patients in comparison to subjects having overdosed on APAP (such as miR-885-5p, Fig 4B). [score:2]
The figure presents serum levels, based on normalized sequencing reads, of significantly altered miRNAs in APAP, HBV, LC, T2DM an HC for miR-122-5p, miR-192-5p, miR-483-5p and miR-194-5p (A) and miR-221-5pp, miR-222-3p, miR-375 and miR-885-5p (B). [score:1]
In fact, only one miRNA (miR-885-5p) was in common for all groups; however, it was increased in APAP, HBV and LC, and decreased in T2DM patients. [score:1]
0177928.g005 Fig 5 The figure presents the isomiR composition, based on normalized mean sequencing reads, in APAP, HBV, LC, T2DM an HC for miR-122-5p (A), miR-194-5p (B), miR-885-5p (C) and miR-221-3p (D). [score:1]
The figure presents the isomiR composition, based on normalized mean sequencing reads, in APAP, HBV, LC, T2DM an HC for miR-122-5p (A), miR-194-5p (B), miR-885-5p (C) and miR-221-3p (D). [score:1]
0177928.g004 Fig 4 The figure presents serum levels, based on normalized sequencing reads, of significantly altered miRNAs in APAP, HBV, LC, T2DM an HC for miR-122-5p, miR-192-5p, miR-483-5p and miR-194-5p (A) and miR-221-5pp, miR-222-3p, miR-375 and miR-885-5p (B). [score:1]
A similar isomiR distribution is presented for miR-194-5p and miR-885-5p in Fig 5B and 5C. [score:1]
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[+] score: 8
For example, post-stroke treatment of rats with valproic acid, a histone deacetylase inhibitor and a mood stabilizer, upregulated the expression of several miRNAs including miR-331 and miR-885-3p, and improved neurological deficits and motor performance following ischemia (115). [score:8]
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[+] score: 8
Q-RT-PCR ΔCt values (y-axis) line plot per animal for duration of Day 1, 7, and 14 treatment samples tested highlights the elevation of both liver enriched miRNAs (miR-122 and miR-885) and ubiquitously expressed miR-193 in the 2 dogs with elevated ALT and AST. [score:3]
Elevations in liver enriched miR-122 and miR-885 correlated with increases in ALT and AST (Fig.   6a and b) and mild to moderate hepatocellular necrosis was observed in 2 of 6 animals (Dogs 1 and 3 on Day 14 [data not shown]). [score:1]
Taken together, these results highlight the specificity of miR-122 and miR-885 for compound -induced liver injury. [score:1]
Dogs with elevated serum levels of miR-122 and miR-885 had a correlative increase of alanine aminotransferase, and microscopic analysis confirmed liver damage. [score:1]
Dogs 1 and 3 had high correlation between elevations in serum miR-122 and ALT (r [2] = 0.79) and AST (r [2] = 0.90) levels while elevations in serum miR-885 were higher ALT (r [2] = 0.87) and AST (r [2] = 0.97). [score:1]
The results from these two POC studies represent the first published data demonstrating the utility of miR-122 and miR-885 as potential biomarkers of liver injury in the dog. [score:1]
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13
[+] score: 8
Cluster 2 miRNAs (light blue) overwhelmingly upregulated p27 phosphorylation and cluster 5 miRNAs upregulated S6 phosphorylation consistent with that which was observed for other members of their respective clusters in screen 1. MiR-885-3p, miR208b and miR-181c* regulated the highest number of components within the phosphoprotein network. [score:8]
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14
[+] score: 7
Among the fifteen miRNAs in the top group, two miRNAs were highly likely to be upregulated, i. e., hsa-miR-24and hsa-miR-885-5p, whereas thirteen miRNAs were highly likely to be downregulated, i. e., hsa-miR-26b, hsa-let-7b, hsa-miR-185, hsa-miR-142-3p, hsa-miR-29b, hsa-miR-483-5p, hsa-miR-144*, hsa-miR-145*, hsa-miR-629*, hsa-miR-222*, hsa-miR-497, hsa-miR-675 and hsa-miR-106b*, in the eutopic endometrium of patients with endometriosis compared with the controls (Table 2). [score:6]
deviation Coefficient of variation Max/min R Mean difference Median difference Mean fold- change Median fold- change1hsa-miR-241.290.043.121.0891.160.086.871.211.111.171.111.172hsa-miR-885-5p4.183.9293.7512.252.061.2359.969.222.021.212.021.213hsa-miR-26b1.380.4331.372.693.043.60118.4812. [score:1]
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15
[+] score: 7
For top 10 upregulated microRNAs (hsa-miR-197-3p, hsa-miR-574-3p, hsa-miR-885-5p, hsa-miR-483-3p, hsa-miR-1281, hsa-miR-328, hsa-miR-4254, hsa-miR-4290, hsa-miR-1825, hsa-miR-766-3p), we included those have been shown to be deregulated in cancer, and have either expression data or functional studies in stem cells. [score:7]
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[+] score: 7
For example, both TargetScan and PACMIT predicted that the DSP in the ABCF1 3′-UTR created a new ssc-miR-34a/c target site while disrupting the ssc-miR-885-3p predicted target site (Table S4). [score:7]
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17
[+] score: 5
Afanasyeva E. A. Mestdagh P. Kumps C. Vandesompele J. Ehemann V. Theissen J. Fischer M. Zapatka M. Brors B. Savelyeva L. MicroRNA miR-885–5p targets CDK2 and MCM5, activates p53 and inhibits proliferation and survival Cell Death Diff. [score:5]
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[+] score: 5
Moreover, the rs1049253 CC genotype was associated with reduced levels of CASP3 mRNA compared with the TT genotype, and C allele resulted in stronger down-regulation than T allele of the CASP3 expression determined with miR-885-5p mimic transfection and luciferase assay [56]. [score:4]
The rs1049253 is a C/T variation located in the 3′UTR of CASP3 gene within the binding site of miR-885-5p. [score:1]
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[+] score: 5
Expression of miR-521, miR-885, and miR-324 in non-neoplastic and neoplastic prostate cells and their exosomes. [score:3]
Levels of miR-521, miR-885, and miR-324 in LNCaP cells, Exo [Hypoxic] and exosomes derived from the serum of PCa patients. [score:1]
RNU6-2 (U6) was used as an internal control and q-PCR results were represented as a fold change relative to normoxic or healthy subjects for miR-521 (A), miR-885 (B) and miR-324 (C). [score:1]
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[+] score: 4
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-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
In a longitudinal study using plasma samples from non-HCV-infected injection drug users who eventually acquired the infection, miR-122 and miR-885-5p were increased in abundance during acute infection, whereas miR-494 and miR-411 were decreased in expression. [score:3]
Furthermore, miR-122 and miR-885-5p levels remained elevated during viremia and returned to preinfection levels after infection resolution (200). [score:1]
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[+] score: 4
044hsa-miR-18b2.20.014hsa-miR-423-5p1.70.048hsa-miR-932.10.014hsa-miR-1911.50.049hsa-miR-548b-5p2.30.015Downregulated miRNAs  hsa-miR-252.10.015hsa-miR-885-5p-4.20.00011hsa-miR-324-3p2.30.017hsa-miR-874-5.80.00018hsa-miR-3262.60.017hsa-miR-486-3p-4.60.00040hsa-miR-18a3.10.017hsa-miR-299-5p-4.20.0020hsa-miR-20b2.00.017hsa-miR-488-3.90.0063hsa-miR-1942.80. [score:4]
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[+] score: 4
EPO Mediates Neurotrophic, Neuroprotective, Anti-Oxidant, and Anti-Apoptotic Effects via Downregulation of miR-451 and miR-885-5p in SH-SY5Y Neuron-Like Cells. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, 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-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-100, hsa-mir-101-1, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-215, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-194-1, hsa-mir-195, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-130b, hsa-mir-302c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-324, hsa-mir-451a, hsa-mir-483, hsa-mir-484, hsa-mir-486-1, hsa-mir-500a, hsa-mir-92b, hsa-mir-595, hsa-mir-596, hsa-mir-421, hsa-mir-378d-2, hsa-mir-744, hsa-mir-939, hsa-mir-940, hsa-mir-1229, hsa-mir-1233-1, hsa-mir-1290, hsa-mir-1246, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-4286, hsa-mir-500b, hsa-mir-1233-2, hsa-mir-3935, hsa-mir-642b, 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-378j, hsa-mir-486-2
They reported that miR-885-5p was significantly elevated in the sera of patients with liver pathologies such as HCC or liver cirrhosis (LC), and their findings indicated the potential of serum miRNAs as novel complementary biomarkers for the detection and assessment of liver pathologies. [score:1]
Gui et al. identified miR-885-5p as a novel biomarker using real-time qPCR -based arrays [42]. [score:1]
They also demonstrated that miR-885-5p correlated with other liver function parameters and hepatic histopathological indicators such as platelets, serum albumin, and the Scheuer grading system in patients with liver pathologies [42]. [score:1]
Several circulating miRNAs, such as miR-27a, miR-642b, miR-885-5p, miR-22, miR-21, miR-483, miR-1246, miR-4644, miR-3976, and miR-4306, have been identified as novel diagnostic markers with acceptable availability in PCa patients [70, 71, 72, 73]. [score:1]
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[+] score: 4
Other miRNAs approaching significance with log2 fold changes up- or downregulation by greater than 1 included miR-10a, miR-133b, miR-138, miR-150, miR-155, miR-212, miR-362-3p, miR-518e, and miR-885-5p. [score:4]
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25
[+] score: 3
83 *** hsa-mir-346 7.13 *** 69.13 *** hsa-mir-361-3p 4.51 *** 9.6 *** hsa-mir-483-3p 3.56 *** 68.61 *** hsa-mir-486-5p 2.85 *** 34.48 *** hsa-mir-574-3p 2.61 *** 43.22 *** hsa-mir-629* 16.62 *** 67.23 *** hsa-mir-885-5p 4.75 *** 43.73 *** Inhibited differentiation & high cell count hsa-mir-193b 38.04 *** 102.74 * Hits of functional screen Relative percentage of myotubes 1, % of control p value, Mann Whitney test Relative cell count 2, % of control p value, Mann Whitney test hsa-mir-369-3p 61.75 *** 103.6 * hsa-mir-381 61.75 *** 105.31 * hsa-mir-886-5p 38.04 *** 112.86 *** hsa-mir-940 21.37 *** 112.35 *** Enhanced differentiation hsa-mir-98 104.51 * 87.82 *** High cell count hsa-mir-631 92.63 ** 103.43 *** 1see Material and Methods; 2 *: p<0.05; **: p<0.01; *** p<0.005; − = not significant. [score:3]
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[+] score: 3
Comparing these results to the study of Qi et al., three miRNAs (miR-25, miR-590-5p, miR-885-5p) were found concordantly and let-7e disconcordantly regulated. [score:2]
miR-22, miR-25, miR-197, miR-365, miR-483-5p, miR-590-5p, and miR-885-5p are yet the most promising candidates since these miRNAs were validated for discrimination of TB and healthy controls in two studies (see Table  2). [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-93, hsa-mir-346
Sandrim V. C. Luizon M. R. Palei A. C. Tanus-Santos J. E. Cavalli R. C. Circulating microRNA expression profiles in pre-eclampsia: Evidence of increased miR-885–5p levelsBJOG Int. [score:3]
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[+] score: 3
Using stringent algorithm, we have identified ten miRNAs (miR-129-5p, miR-3148, miR-4470, miR-4672, miR-3646, miR-3180, miR-4690, miR-3622, miR-5096, and miR-885) that can target different genes in innate immune pathway. [score:3]
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[37] For example, ULK1 (unc-51 like autophagy activating kinase 1) is targeted by MIR20A and MIR106; [85] BECN1/beclin 1 by MIR30A, MIR376B and MIR519A; [86-89] RAB5A (RAB5A, member RAS oncogene family) by MIR101 and MIR630; [89,90] RB1CC1/FIP200 (RB1 inducible coiled-coil 1) by MIR224; [91] and ATGs by MIR30A, MIR181A, MIR374A, MIR630, MIR376B, MIR204, MIR224, MIR375, MIR519A, MIR885, and MIR-101. [score:3]
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[+] score: 3
In a subsequent study, the expression of 380 miRNAs using TaqMan low density arrays was evaluated in the plasma of patients with primary osteoarthritis and controls and 12 miRNAs (hsa-miR-16, hsa-miR-20b, hsa-miR-29c, hsa-miR-30b, hsa-miR-93, hsa-miR-126, hsa-miR-146a, hsa-miR-184, hsa-miR-186, hsa-miR-195, hsa-miR-345, and hsa-miR-885) were identified being over-expressed in OA patients [28]. [score:3]
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[+] score: 2
Plasma miR-22-3p, miR-642b-3p, and miR-885-5p were also shown to have high sensitivity in the diagnosis of early stage PDA together with CA19-9 [112]. [score:1]
Hussein N. A. Kholy Z. A. Anwar M. M. Ahmad M. A. Ahmad S. M. Plasma miR-22-3p, miR-642b-3p and miR-885-5p as diagnostic biomarkers for pancreatic cancer J. Cancer Res. [score:1]
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Meier C, Hardtstock P, Joost S, Alla V, Pützer (2016) BM2p73 and IGF1R regulate emergence of aggressive cancer stem-like features via miR-885-5p control. [score:2]
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Ten of the miRNAs in Table 2 have been identified with at least 10 reads and four of these (miR-151, miR-885, miR-140 and miR-520a) also have corresponding star reads of lower abundance. [score:1]
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73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32. [score:1]
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For example, the 3’ arm of hsa-mir-885 with its downstream sequence is derived from 2 bp to 192 bp of AluSc. [score:1]
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Four other miRNAs, representing homologs of miR-337, miR-377, miR-513c and miR-885 respectively, were also confirmed to have novel seed sequences in P. alecto. [score:1]
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Other miRNAs from this paper: hsa-mir-302b, hsa-mir-629, hsa-mir-936, hsa-mir-1324, hsa-mir-323b
[a]This new SNV found in hsa-mir-885/hsa-miR-885-3p was experimentally confirmed (Table 2). [score:1]
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011  hsa-mir-885-5p −4.304. [score:1]
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