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33 publications mentioning hsa-mir-505

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-505. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 269
In this study, overexpression of miR-505 downregulated both MMP2 and MMP9 mRNA and protein expression, providing further evidence that upregulation of miR-505 may inhibit invasion and metastasis in EC. [score:13]
Furthermore, RT-PCR and demonstrated that overexpression of miR-505 downregulated the mRNA (Fig.   6a, P < 0.05) or protein (Fig.   6b, P < 0.05) expression of MMP2, MMP9, CDK2, and TGF-α, while upregulated Bax and cleaved PARP expression in both cells. [score:13]
Therefore, these results indicate that upregulation of miR-505 promotes apoptosis in EC by upregulating Bax and PARP and inducing G1-S stage arrest via downregulation CDK2. [score:10]
We infer that upregulation of miR-505 may inhibit proliferation, migration and invasion; promote apoptosis in EC by leading to decreased expression of TGF-α. [score:8]
A miR-505 binding site was identified in the 3′ untranslated region of TGF-α mRNA (TGFA) using miRNA target-detecting software; a dual luciferase reporter assay confirmed that miR-505 directly targets and regulates TGFA. [score:8]
RT-PCR and Western-blotting results indicated that overexpressing miR-505 reduced the expression of TGF-α and the TGF-α-regulated proteins MMP2, MMP9, CDK2, while induced Bax and cleaved-PARP expression in EC cells. [score:8]
In this study, overexpression of miR-505 reduced CDK2 mRNA and protein expression, upregulated Bax and increased the levels of cleaved PARP. [score:8]
miR-505 directly targets TGFA and regulates TGF-α expression in EC cells. [score:7]
Additionally, overexpression of miR-505 significantly inhibited EC cell proliferation, induced G1-S arrest and apoptosis, and suppressed EC cell invasion and migration in vitro. [score:7]
miR-505 overexpression reduced TGF-α, CDK2, MMP2 and MMP9 expression, while increased cleaved PARP and Bax mRNA (a) or protein (b) expression. [score:7]
Here, we report that miR-505 functions as a tumor suppressor in EC by targeting and regulating TGFA. [score:6]
Immunohistochemical analysis demonstrated a significant reduction of TGF-α expression in the HSA-miR-505 group (b) compared with the mock group (a) in nude mice tumor tissues This study demonstrates that miR-505 is significantly downregulated in human EC compared to normal endometrial tissues, and the expression of miR-505 was significantly associated with the FIGO stage and lymph node metastasis. [score:6]
Overexpression of miR-505 inhibits proliferation, induces apoptosis and reduces the tumorigenicity of EC cells in vitro. [score:5]
are representative of three separate experiments; data are expressed as the mean ± standard deviation, * P < 0.05 We analyzed the mRNA sequence of TGF-α using the miRNA target-detecting software and identified binding sites for miR-505 in TGFA (Fig.   5a). [score:5]
In vivo, overexpression of miR-505 reduced the tumorigenicity and inhibited the growth of xenograft tumors in a mouse mo del of EC. [score:5]
In confirmation of this functional interaction, overexpression of miR-505 reduced both TGF-α mRNA and protein expression in EC cell lines. [score:5]
Taken together, this data indicates that downregulation of miR-505 could promote the development and progression of EC. [score:5]
In conclusion, we demonstrate that miR-505 suppresses cell proliferation, invasion and metastasis in EC by targeting TGFA. [score:5]
These results provide further confirmation that miR-505 might act as tumor suppressor in EC by targeting TGFA. [score:5]
Fig. 7Overexpression of miR-505 inhibits the growth of tumor xenografts in a mouse mo del. [score:5]
Overexpression of miR-505 significantly inhibited tumor xenograft growth and led to a reduced tumor volume. [score:5]
In vitro, overexpression of miR-505 significantly suppressed EC cell proliferation, increased apoptosis and reduced migratory and invasive activity. [score:5]
Overexpression of miR-505 inhibits the growth of EC xenografts in a mouse mo del. [score:5]
In this study, target prediction software identified a miR-505 binding site in the 3′ UTR of TGFA, and dual-luciferase reporter assays confirmed that TGFA is a direct target of miR-505. [score:5]
Taken together, this study demonstrates that miR-505 acts as tumor suppressor in EC by regulating TGF-α. [score:4]
Immunohistochemical analysis demonstrated a significant reduction of TGF-α expression in the HSA-miR-505 group (b) compared with the mock group (a) in nude mice tumor tissues Quantitative reverse transcription polymerase chain reaction (qRT-PCR) demonstrated that miR-505 was expressed at lower levels in human EC than normal endometrial tissues (Fig.   1a, b, P < 0.05, 1: Table S1). [score:4]
The tumors formed by the cells overexpressing miR-505 had a significantly lower TGF-α expression compared to the mock group (Fig.   8a and b). [score:4]
Associations between miR-505 expression and the clinicopathological features of EC. [score:3]
miR-505 expression in normal endometrial and endometrial. [score:3]
miR-505 mRNA expression was significantly lower in endometrial adenocarcinoma than in normal endometrial tissues (a- b), and was negatively associated with FIGO stages (c), and Lymph node metastasis (d). [score:3]
RT-PCR results demonstrated that miR-505 was significantly downregulated in human EC tissues compared to normal endometrial tissues. [score:3]
HEK293T cells were seeded into 24-well plates, cotransfected with 50 nM miR-505 or scrambled mimic and 600 ng of dual luciferase vector expressing the wild-type or mutant 3′-UTR TGF-α sequences. [score:3]
IHC staining confirmed that the tumors formed by miR-505 -transfected cells expressed lower levels of TGF-α. [score:3]
miR-505 expression in normal endometrial tissue, endometrial carcinomas were quantified by Quantitative reverse transcription PCR. [score:3]
Expression of miR-505 correlates with established prognostic biomarkers in breast cancer [22]. [score:3]
Besides, miR-505 expression was negatively associated with FIGO stage (Fig.   1c, stage I/II vs. [score:3]
Correlation of miR-505 expression with different clinicopathological features of endometrial carcinoma. [score:3]
To determine whether miR-505 affected the expression of TGF-α in vivo, we performed immunohistochemical staining of the excised xenograft tumors. [score:3]
are representative of three separate experiments; data are expressed as the mean ± standard deviation, * P < 0.05 Fig. 4Effects of miR-505 transfection on invasive and metastatic ability of endometrial adenocarcinoma cell lines in vitro. [score:3]
are representative of three separate experiments; data are expressed as the mean ± standard deviation, * P < 0.05 Fig. 6Effects of miR-505 transfection on endometrial adenocarcinoma cell genotype in vitro. [score:3]
However, little is known about the biological function and target genes of miR-505 in EC. [score:3]
There were no significant associations between miR-505 expression and the depth of invasion and pathological type (endometrial adenocarcinoma vs. [score:3]
and a xenograft mouse mo del were used to examine miR-505 and its target gene TGF-α. [score:3]
Quantitative reverse transcription polymerase chain reaction (qRT-PCR) demonstrated that miR-505 was expressed at lower levels in human EC than normal endometrial tissues (Fig.   1a, b, P < 0.05, 1: Table S1). [score:3]
Another study recently provided evidence that miR-505 could suppress the epithelial-mesenchymal transition (EMT) and metastasis in nasopharyngeal carcinoma [23]. [score:3]
Numerous studies have indicated that miR-505 inhibits cell proliferation by inducing apoptosis and can promote chemoresistance in breast cancer [18, 21]. [score:3]
Besides, miR-505 expression was negatively associated with FIGO stage (stage I-II vs. [score:3]
Furthermore, cytometry flow showed that overexpression of miR-505 induced significant G1 phase arrest (Fig.   3a, P < 0.05; PI staining) and high levels of apoptosis (Fig.   3b, P < 0.05, Annexin V-FITC and PI staining). [score:3]
Fig. 1Associations between miR-505 expression and the clinicopathological features of EC. [score:3]
The CCK-8 assay demonstrated that the miR-505 overexpression (Fig.   2a, P < 0.05) significantly inhibited cell proliferation in both cell lines compared with the mock or negative control group (Fig.   2b, P < 0.05). [score:3]
Luciferase assays were carried out to confirm the interaction between miR-505 and the 3′ untranslated region (UTR) of TGFA. [score:2]
Compared to the mock group, HEC-1B cells overexpressing miR-505 had a significantly lower tumor volume (Fig.   7a and b, P < 0.05) and slower rate of growth (Fig.   7c, P < 0.05). [score:2]
miR-505 overexpression reduced cell migration (a), and invasion ability (b) compared with the control and mock cells. [score:2]
MiR-505 has been identified to function as a tumor suppressor in breast cancer [18– 20]. [score:2]
The endometrial carcinoma cell lines HEC-1B and Ishikawa were each transfected with miR-505 or scrambled mimics, after which cell phenotype and expression of relevant molecules were assayed. [score:2]
miR-505 transfection exhibited significantly higher miR-505 expression (a) and slower growth ability (b) compared with the control and mock cells. [score:2]
Tumor xenograft volume in nude mice treated with miR-505 was smaller than that in mock nude mice (a and b). [score:1]
EC cells were transfected with miR-505 mimic or scrambled mimic, seeded into 96-well plates (2 × 10 [3] cells per well) and incubated until adherent. [score:1]
Cells transfected with miR-505 mimic or mock mimic were collected after 48 h, re-suspended in serum-free DMEM medium, and 5 × 10 [4] cells in serum-free medium were seeded into the upper chamber of Transwell inserts that had been pre-coated with Matrigel (40 μL of 8 mg/mL stock solution; Becton-Dickinson Labware, Bedford, MA, USA); normal culture medium was placed into the lower chamber. [score:1]
EC = endometrial adenocarcinoma, * P < 0.05 Ishikawa and HEC-1B cell lines were transfected with miR-505 mimic or the scrambled mimic. [score:1]
We analyzed the mRNA sequence of TGF-α and identified binding sites for miR-505 in TGFA. [score:1]
Hairpin-it™ microRNA and U6 snRNA Normalization RT-PCR Quantitation (GenePharma) was used to check mature miR-505 in cells. [score:1]
The predicted seed region in the 3′ UTR of TGF-α (a); Luciferase activity is unchanged when using a scrambled miRNA sequence or miR-505 with the mutant 3′-UTR of TGF-α. [score:1]
However, when the wild-type 3′-UTR of TGF-α is used, the promoter activity is significantly reduced by miR-505 (b). [score:1]
Moreover, data from mouse mo dels has indicated an association between miR-505 and human basal-type breast cancer [19]. [score:1]
Additionally, overexpression of miR-505 significantly reduced the invasion (Fig.   4a, P < 0.05, Transwell assay) and migratory ability of both cell lines (Fig.   4b, P < 0.05, wound healing assay). [score:1]
The miR-505 mimic sequence was GGG AGC CAG GAA GUA UUG AUG U, and the scrambled mimic (Mock) sequence was ACU ACU GAG UGA CAG UAG A. The scrambled mimic was also transfected in cells as negative control. [score:1]
An in vivo mo del of EC was established by subcutaneously injecting 5-week-old female BALB/c nude mice with 1 × 10 [7] HEC-1B cells transfected with miR-505 (or mock transfected) suspended in PBS (10 mice per group). [score:1]
Recent studies have demonstrated that miR-505 is associated with several types of cancer; however, the expression and function of miR-505 have not been investigated in EC. [score:1]
Cells were collected 48 h after transfection, washed twice with cold PBS, and resuspended at 1 × 10 [6] cells/mL and mixed with 100 μL of 1× buffer and 5 μL Annexin V- PE and 7AAD, incubated for 15 min in the dark, 400 μL 1× buffer was added, and the cells were subjected to cytometry flow within 1 h. Cells were seeded into 6-well plates, allowed to adhere and transfected with miR-505 mimic or scrambled mimic, linear wounds were created in the confluent monolayers using a pipette tip. [score:1]
Cells were each transfected with miR-505 mimic using Lipofectamine 2000 reagent (Invitrogen, Carlsbad, USA) according to the manufacturer’s protocol. [score:1]
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2
[+] score: 137
As for gene expression data, since the expression level of miRNA -regulating genes was up-regulated when miRNA expression was lower in MCF7-ADR than in MCF7 cells, up-regulated genes judged by the T-test (1, 758 genes, Additional File 10 Table S5) were selected as candidates of miR-505. [score:14]
Using a gain of function study with 12 miRNAs whose expressions were down-regulated and genome regions were deleted, we show that miR-505 is a novel tumor suppressive miRNA and inhibits cell proliferation by inducing apoptosis. [score:10]
S6), indicating that down-regulation of Akt3 after miR-505 overexpression was caused by indirect effect of miR-505 -mediated gene suppression. [score:9]
We found that the expression of miR-505 was down-regulated, and its genomic region was deleted in MCF7-ADR cells, which provided evidence that miR-505 was a tumor suppressive miRNA and had a pivotal role for inducing apoptosis in drug resistant cancer cells. [score:8]
In addition, of 12 miRNAs whose expressions were down-regulated and genomic regions were deleted, we determined that miR-505 promotes the inhibition of cell growth in MCF7-ADR cells, by inducing apoptotic cell death in the presence of docetaxel (DOC). [score:8]
Our studies by means of an integrated genomic analysis not only identified miR-505 as a tumor suppressive miRNA that inhibited cell proliferation by inducing apoptotic cell death but also, more broadly highlighted that various genes and miRNAs orchestrate to temper the drug resistance by intricately controlling genomic status, gene and miRNA expression in cancer cells. [score:7]
As shown in Figure 6B, decrease in relative gene expression was observed with miR-505 in MCF7-ADR-Luc cells, suggesting that miR-505 suppresses the gene expression of Akt3. [score:7]
In addition, by using the data of gene expression and bioinformatics analysis (gene function), our data identified Akt3 whose expression was conversely correlated with miR-505, which modulated drug sensitivity in MCF7-ADR. [score:5]
A 1235 bp fragment from the 3'UTR of Akt3 containing the predicted target sequence of miR-505 (located at positions 529-535 of the Akt3 3'UTR) and a 934 bp fragment from the 3'UTR of Akt3 containing the predicted target sequence of miR-505 (located at positions 529-535 of this fragment) were PCR-cloned from MCF7-ADR cells isolated total RNA. [score:5]
These data suggest that miR-505 is a novel tumor suppressive miRNA and plays a role in the regulation of cell proliferation similar to let-7d. [score:4]
Therefore, our data show that Akt3, whose expression is correlated conversely with miR-505, regulates DOC sensitivity in MCF7-ADR cells. [score:4]
Inversely, transfection of miR-505 and let-7d inhibited the cell proliferation of MCF7-ADR-Luc cells. [score:3]
Figure 6 Akt3, whose expression was inversely correlated with miR-505, is associated with drug resistance in MCF7-ADR cells. [score:3]
Inhibitory effects of cell growth by miR-505 and let-7d transfection are at similar level (Figure 4F). [score:3]
Given this evidence and the observed phenotype in miR-505 -transfected MCF7-ADR-Luc cells, we sought to determine whether Akt3 was a target of miR-505 or not. [score:3]
Akt3, correlates inversely with miR-505 expression, modulates drug sensitivity. [score:3]
miR-505 inhibits cell growth by inducing apoptotic cell death in MCF7-ADR cells. [score:3]
To investigate what kind of the genes are responsible for the drug sensivity by miR-505 induce gene suppression, we combined gene expression data and gene ontology (Figure 6A). [score:3]
As miR-505 -targeted genes, apoptosis-related genes (153 genes, Additional File 11 Table S6) were chosen using a database (KEGG web site, http://www. [score:3]
However, our results showed that inhibition of Akt3 was less effective than transfection of miR-505 in cell growth arrest. [score:3]
Figure 5 miR-505 inhibits cell growth by inducing apoptotic cell death in MCF7-ADR. [score:3]
The expression level of miR-505 was also decreased by real-time RT-PCR analysis in MCF7 and MCF7-ADR cells (Figure 5C). [score:3]
Taqman probes for human were used to assess the expression levels of miRNAs (hsa-miR-505, ID: 4373230, hsa-miR-130, ID: 000454, and hsa-miR-155, ID: 002623). [score:3]
Seventy-two hours after transfection with miR-505 or control miRNA, Akt3 expression levels were determined. [score:3]
Taken together, we concluded that transfection of miR-505 inhibit the growth of drug resistance cells, MCF7-ADR, through the inducing apoptosis. [score:3]
To further examine the mechanism of cell growth inhibition, we sought to check whether miR-505 is responsible for cell apoptosis in MCF7-ADR cells. [score:3]
By combining these data, we postulated that Akt3 gene is candidate of miR-505 -regulating gene, which is responsible for the drug resistance in breast cancer cell (Figure 6A). [score:2]
jp/kegg/) because transfection of miR-505 induced apoptotic cell death in MCF7-ADR-Luc cells. [score:1]
Seventy-two hours after transfection with miR-505 (top) or control miRNA (bottom), condensed and fragmented cells are observed. [score:1]
We also find that Akt3, correlate inversely with miR-505, modulates drug sensitivity in MCF7-ADR. [score:1]
However, we found that miR-505 could not bind to the 3'-UTR of Akt3 gene (Additional File 12 Figure. [score:1]
From the aCGH data, genomic region of miR-505 locus in MCF7-ADR was deleted (Figure 5B), in contrast it was intact in MCF7. [score:1]
We validated this result by counting the Hoechst-stained cells showing apoptotic nuclear condensation and fragmentation and found that significantly higher apoptotic cell death was observed in cells with miR-505 than in control miRNA (p < 0.05, Figure 5E and 5F). [score:1]
Since transfection of miR-505 showed the inhibition of cell proliferation effectively and significantly (Figure 4F and 5A), we focused on miR-505 to evaluate its molecular function in this study. [score:1]
Seventy-two hours after transfection, caspase-7 activity in the presence or absence of DOC (1 nM) was detected in miR-505 or control miRNA -transfected MCF7-ADR cells. [score:1]
The 12 miRNAs (miR-23b, miR-25, miR-27b, miR-93, miR-106b, miR-189, miR-489, miR-505, miR-542-5p, miR-565, miR-652, and let-7d) were transfected into MCF7-ADR-Luc cells (Figure 4F). [score:1]
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3
[+] score: 35
Interestingly, Qin et al. have reported that miR-505 is upregulated in a nasopharyngeal cell line but that miR-505 surprisingly still inhibits metastasis and suppresses the expression of EMT markers, which are the genes associated with cell migration and invasion [71]. [score:10]
Additionally, several reports have indicated that miR-505 plays a suppressor role in cervical carcinoma by targeting the Frizzled-4 gene (FZD4) [68] and in endometrial cancer by targeting transforming growth factor- α (TGF- α) [69]. [score:7]
However, high expression of miR-505 is strongly associated with a poor prognosis in lymph node -negative breast cancer patients [67]. [score:3]
miR-505 attenuates HCC cell proliferation and invasion by inhibiting HMGB1, suggesting potential antitumor roles for miR-505 in HCC [39]. [score:3]
miR-505 is reportedly associated with apoptosis, and studies of drug-resistant human breast cancer cell lines have shown that miR-505 inhibits proliferation by inducing apoptosis [66]. [score:3]
miR-505 expression is correlated with the potential of establishing a biomarker of the imatinib therapeutic response in chronic myeloid leukemia patients [70]. [score:3]
Dysregulation of miR-505 might be associated with HCC [72]. [score:2]
Several studies discuss the role of miR-505 in different cancers. [score:1]
A recent article has presented several studies showing that miR-505 is decreased in various HCC cell lines. [score:1]
Similarly, the results of studies in HCC have also revealed several latent functions for miR-505. [score:1]
3.3. miR-505. [score:1]
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4
[+] score: 29
Other miRNAs from this paper: hsa-mir-197, hsa-mir-145, hsa-mir-129-2, hsa-mir-328, hsa-mir-1207
b Heat map showing strength and directionality of associations between pleiotropic mRNA and miRNAs Gene ontology enrichment analysis (Additional file 1: Table S15) revealed that the co-expressed mRNAs for miR-505-5p were enriched for genes involved in RNA metabolism (P = 3.5 × 10 [−5]). [score:4]
b Heat map showing strength and directionality of associations between pleiotropic mRNA and miRNAs Gene ontology enrichment analysis (Additional file 1: Table S15) revealed that the co-expressed mRNAs for miR-505-5p were enriched for genes involved in RNA metabolism (P = 3.5 × 10 [−5]). [score:4]
These highly pleiotropic miRNAs were associated with a large number of mRNAs (1109 mRNAs in total; 396 coexpressed mRNAs for miR-505-5p, 241 for miR-197-3p, 177 for miR-145-5p, and 649 for miR-328). [score:3]
Gene ontology enrichment analysis (Additional file 1: Table S15) revealed that coexpressed mRNAs for the most pleiotropic miRNAs were enriched for RNA metabolism (miR-505-5p), ubiquitin -dependent protein catabolism (miR-197-3p and miR-328), and chromatin assembly (miR-328). [score:3]
As with miR-505-5p, miR-145-5p is highly expressed in smooth muscle cells and controls smooth muscle cell differentiation and function, particularly in the context of metabolic syndrome [32]. [score:3]
As shown in Table  3, the top gene target of miR-505 is major histocompatibility complex, class I (MR1). [score:3]
miR-505-5p targets SRSF1 (Serine/arginine-rich splicing factor 1). [score:3]
mRNAs coexpressed with pleiotropic miRNAs were enriched for RNA metabolism (miR-505-5p), ubiquitin -dependent protein catabolism (miR-197-3p, miR-328) and chromatin assembly (miR-328). [score:3]
miRNAs miR-505-5p, miR-197-3p, miR-145-5p, and miR-328 exhibited significant associations with BMI, SBP, DBP, and TG. [score:1]
Fifty miRNAs were associated with three or more CM traits and four were associated with four CM traits (miR-197-3p, miR-328, miR-505-5p, miR-145-5p) (Table  3 and Fig.   1). [score:1]
Four mRNAs (FAM13A, CSF2RB, HIST1H2AC, WNK1) were associated with all 6 CM traits (FDR < 0.001) and four miRNAs (miR-197-3p, miR-328, miR-505-5p, miR-145-5p) were associated with four CM traits (FDR < 0.05). [score:1]
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5
[+] score: 26
A comparison was performed between the miRNAs upregulated in both MMTBI and STBI group which identified a signature of 10 miRNAs viz miR-151-5p, miR-195, miR-20a, miR-328, miR-362-3p, miR-30d, miR-451, miR-486, miR-505* and miR-92a, with increased expression in both MMTBI and STBI groups (Fig. 2, Common miRNAs in MMTBI and STBI are highlighted in bold in Tables 1 and 2). [score:6]
MiR-505* and miR-451 were not predicted to target any of the target molecules for TBI in IPA. [score:5]
For miR-505* and miR-195, although the mean fold upregulation was more than 10 fold, however it was only observed in 50–60% of the samples whereas in the remaining samples it was not detected, hence these failed the statistical test. [score:4]
MiR-505* and miR-195 were upregulated however due to sample outliers in a small group it was not statistically significant. [score:4]
We randomly selected five miRNAs miR-195, miR-328, miR-362-3p, miR-486 and miR-505* and performed specific miRNA assays to validate their expression. [score:2]
The real time data for miR-151-5p, miR-195, miR-20a, miR-30d, miR-328, miR-362-3p, miR-451, miR-486, miR-505* and miR-92a was normalized using miR-202. [score:1]
There were significant differences between the two groups for all but two of the selected miRNA: miR-195 (p < 0.001); miR-30d (p < 0.001); miR-451 (p < 0.011); miR-328 (p < 0.101); miR-92a (p < 0.001); miR-486 (p < 0.006); miR-505 (p < 0.008); and miR-362 (p < 0.035); miR-151 (p < 0.065); and miR-20a (p < 0.012) (Fig. 5). [score:1]
The AUC’s were: miR-195 (0.81), miR-30d (0.75), miR-451 (0.82), miR-328 (0.73), miR-92a (0.86), miR-486 (0.81), miR-505 (0.82), miR-362 (0.79), miR-151 (0.66), miR-20a (0.78). [score:1]
The analysis identified the AUC values as miR-195 (0.81, p value < 0.003), miR-30d (0.75, p value < 0.016), miR-451 (0.82, p value < 0.002), miR-328 (0.73, p value < 0.030), miR-92a (0.86, p value < 0.001), miR-486 (0.81, p value < 0.003), miR-505 (0.82, p value < 0.002), miR-362 (0.79, p value < 0.006), miR-151 (0.66, p value < 0.123), miR-20a (0.78, 0.007). [score:1]
There were significant differences between the two groups for all but two of the selected miRNA (see asterisks): miR-195 (p < 0.001); miR-30d (p < 0.001); miR-451 (p < 0.011); miR-328 (p = 0.101); miR-92a (p < 0.001); miR-486 (p = 0.006); miR-505 (p = 0.008); and miR-362 (p = 0.035); miR-151 (p = 0.065); and miR-20a (p = 0.012). [score:1]
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[+] score: 25
Time -dependent expression of miR-122, miR-192, miR-21, miR-29a, miR-34a, and miR-505 in study 1. Data were expressed as minus delta Ct with reference to spike-in control miRNA. [score:5]
MicroRNA profiling in two independent cohorts of animals validated the up-regulation of 6 microRNAs (miR-122, miR-192, miR-21, miR-29a, miR-34a and miR-505) in NASH mice, which was designated as the circulating microRNA signature for NASH. [score:4]
Notably, we detected significant up-regulation of liver miR-21, miR-34a and miR-505 in NASH mice compared to lean mice (data was not shown). [score:3]
The right panel depicted the expression level of miR-192 and miR-505 in mice having NAS > 3 compared with mice having NAS ≤ 3. c ROC curves of the microRNA signature in predicting mice having NAS > 3 (AUC = 0.897, 95% confidence interval: 0.75 - 1) in study 1. The confusion matrix was depicted in the inset (numbers in rows are actual classification, numbers in columns are predicted classification). [score:2]
MiR-505 was selected because of its high correlations with disease pathologies (NAS, r = 0.77), but relatively low associations with other microRNAs. [score:2]
a, b Univariate ROC analysis of miR-192 and miR-505, which was created by plotting the true positive rate (sensitivity) against false positive rate (1-specificity). [score:1]
c Principle component analysis (PCA) of miR-192, miR-122, miR-21, miR-29a, miR-34a, and miR-505 in study 2. Red dots represented NASH mice (mice on 3H diet for 7 months), and green dots represented lean mice. [score:1]
b, c ROC curves of the miR-192, miR-21, miR-505 and ALT in predicting mice having NAS > 3 in study 1 (AUC = 0.948, 95% confidence interval: 0.827 - 1) and study 3 (AUC = 0.931, 95% confidence interval: 0.845 - 1). [score:1]
We then tested the performance of the new composite biomarker consisting of miR-192, miR-505, miR-21 and ALT in discriminating NASH animals (NAS > 3) from healthy mice (NAS ≤ 3) in study 1 and 3. As shown in Fig.   5b, the new biomarker outperformed the microRNA signature plus ALT mo del, and achieved AUROC of 0.958 with further reduction of one misclassified animal in study one. [score:1]
The top six common microRNAs including miR-21, miR-122, miR-192, miR-29a, miR-34a and miR-505, were designated as the circulating microRNA signature for NASH (Fig.   2b). [score:1]
Based on these findings, a microRNA -based composite biomarker consisting of miR-192, miR-21, miR-505 and ALT was proposed, which demonstrated great performance in distinguishing between lean and NASH mice (NAS > 3). [score:1]
To further improve the performance of microRNA -based biomarker, a new composite biomarker was proposed, which consists of miR-192, miR-21, miR-505 and ALT. [score:1]
Univariate ROC curve analysis showed that miR-192 and miR-505 achieved the greatest AUROC of 0.923 and 0.919 respectively in discriminating mice had NAS > 3, while miR-122, miR-29a, miR-34a and miR-21 had an AUROC of 0.88, 0.84, 0.80 and 0.79 (Fig.   4a and b). [score:1]
In view of the biological function of each feature, the new composite biomarker could potentially reflect the status of the liver from the following perspectives: miR-192 and ALT serve as independent indicator of hepatocyte function, miR-21 suggests of stellate cell activation and liver fibrosis, miR-505 implies for pathological manifestations. [score:1]
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7
[+] score: 11
GWAS SNP miRNA target site SNP CHR BP Distance to GWAS SNP miRNA target site SNP alleles LD R2 microRNA Target gene Target transcript rs113948889 rs112215626 12 2,059,337 44,833 G/A 1 hsa-miR-4775 DCP1B ENST00000540622 rs113948889 rs1044950 12 2,061,982 42,188 T/C 1 hsa-miR-138-5p DCP1B ENST00000541700 rs113948889 rs34730825 12 2,064,602 39,568 C/T 1 hsa-miR-3147 DCP1B ENST00000543381 rs113948889 rs111963484 12 2,102,086 2,084 C/A 1 hsa-miR-4270 DCP1B ENST00000535873 rs113948889 rs111963484 12 2,102,086 2,084 C/A 1 hsa-miR-4441 DCP1B ENST00000535873 rs113948889 rs111963484 12 2,102,086 2,084 C/A 1 hsa-miR-505-5p DCP1B ENST00000535873 rs113948889 rs112637373 12 2,102,271 99 G/T 1 hsa-miR-2909 DCP1B ENST00000535873 rs113948889 rs34730825 12 2,064,602 39,568 C/T 1 hsa-miR-92a-1-5p DCP1B ENST00000543381 Legend: Predicted miRNA target site SNPs in linkage disequilibrium with GWAS SNP rs113948889 listed in descending order of predicted effect on miRNA-to-mRNA binding. [score:11]
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8
[+] score: 11
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-139, 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, 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
Cluster 1, composed by miR-674-3p, miR-505-3p and miR-212-5p, was up-regulated during epileptogenesis (4 and 8 days after SE). [score:4]
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]
Even if displaying the same patterns observed with the microarray, the expression levels of mir-181c-5p, miR-433-3p, miR-505-3p and miR-551b-3p were not significantly different from controls (Fig. 4). [score:3]
Cluster 4, together with cluster 1 (that includes miR-674-3p, miR-505-3p and miR-212-5p) and cluster 5 (including miR-144b-5p and miR-20b-5p), may also strongly influence neuronal activity. [score:1]
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9
[+] score: 10
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-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-505 acts as a tumor suppressor by inhibiting proliferation and inducing apoptosis of human breast cancer cells (Yamamoto et al., 2011). [score:4]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREB MiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREBMiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
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10
[+] score: 10
Six miRNAs were overexpressed (hsa-miR-193a-3p, hsa-miR-29b-1-5p, hsa-miR-505-5p, hsa-miR-194-5p, hsa-miR-99b-3p, and hsa-miR-200b-3p) and 14 (hsa-miR-3663-3p, hsa-miR-513a-5p, hsa-miR-146b-5p, hsa-miR-1972, hsa-miR-718, hsa-miR-3138, hsa-miR-21-5p, hsa-miR-630, hsa-miR-575, hsa-miR-301a-3p, hsa-miR-636, hsa-miR-34a-3p, hsa-miR-21-3p, and hsa-miR-516a-5p) were downregulated in aortic tissue from AS patients (Table 2). [score:6]
Six overexpressed miRNAs (hsa-miR-193a-3p, hsa-miR-29b-1-5p, hsa-miR-505-5p, hsa-miR-194-5p, hsa-miR-99b-3p, and hsa-miR-200b-3p) and 14 downregulated miRNAs (hsa-miR-3663-3p, hsa-miR-513a-5p, hsa-miR-146b-5p, hsa-miR-1972, hsa-miR-718, hsa-miR-3138, hsa-miR-21-5p, hsa-miR-630, hsa-miR-575, hsa-miR-301a-3p, hsa-miR-636, hsa-miR-34a-3p, hsa-miR-21-3p, and hsa-miR-516a-5p) were identified in patients with AS, relative to normal controls, and their general characteristics and functional annotations were analyzed using bioinformatic tools. [score:4]
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11
[+] score: 9
The constructed networks from significantly up-regulated miRNAs and significantly down-regulated target genes involved 13 miRNAs from JIA (Fig. 4a) and 29 miRNAs from CF (Fig. 4b), 4 (miR-494, miR-370, miR-326, and miR-505) of them were common (p = 1.2E-03, Table S4 in Supplementary information). [score:9]
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12
[+] score: 7
Furthermore, miR-505 seems to be regulated by its predicted target Akt3 (an anti-apoptotic gene), by mRNA profiling coupled with downstream validation studies. [score:4]
miR-505 was identified as a tumour suppressor, whose genomic region was found to be deleted in doxorubicin-resistant cells. [score:3]
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[+] score: 6
Besides the metabolic pathways, recent studies have shown that micro RNAs, such as miR-122, miR-192, miR-21, miR-29a, miR-34a, and miR-505, are up or down regulated at disease state of NASH and may play a role in the disease progression (Liu et al., 2018). [score:6]
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14
[+] score: 5
Similar inhibitory mechanisms (targeting MDV in this case) have been reported for miR-23, miR-378, and miR-505 (133). [score:5]
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[+] score: 5
S3 DatasetLog2-transformed miRNA expression ratios obtained from RT-qPCR analysis are plotted for the most reliable (RF ≥ 0.8) miRNAs from set A: (A) miR-100, (B) miR-146a, (C) miR-1274B and the most informative (MoR-value d≥0.57) miRNAs from set B: (D) miR-505*, (E) miR-375, and (F) miR-103. [score:3]
Moreover, we could also confirm the 9 informative miRNAs (miR-505-5p, miR-4467, miR-766, miR-375, miR-708, miR-3622b-3p, miR-296, miR-219 and miR-103) from set B as significant biomarkers by MANCOVA all reaching Bonferroni corrected significance. [score:1]
The MoR plot illustrates the 9 most informative miRNAs, hsa-miR-505-5p, hsa-miR-4467, hsa-miR-766, hsa-miR-375, hsa-miR-708, hsa-miR-3622b-3p, hsa-miR-296, hsa-miR-219 and hsa-miR-103, each reaching a MoR value ≥ 0.57 (critical MoR value on the information chain). [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-98, hsa-mir-141, hsa-mir-143, hsa-mir-551b, hsa-mir-652
Of these, miR-505, miR-652 and miR-551b* demonstrate the most robust associations. [score:1]
However, when assessed using sequencing data, the hazard ratio for mir-505 was 0.998 (p = 0.03). [score:1]
0087782.g002 Figure 2 (A) miR-98, (B) miR-505 (C) miR-143 and (D) miR-141. [score:1]
For example, miR-505 is the miRNA most robustly associated with patient outcome in our analyses of the miRNA array data (HR = −1.7, p<9e-5). [score:1]
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[+] score: 4
Three miRNAs associated with human basal-type tumors (miR-135b, miR-505 and miR-155), and seven miRNAs associated with human luminal type tumors (let-7a, let-7f, miR-100, miR-130a, miR-152, miR-214 and miR-29b) are similarly expressed in mouse basal-like and luminal-type tumors, respectively. [score:3]
miR-135b, miR-505 and miR-155 are expressed in both basal human and mouse mammary tumors and many basal -associated miRNAs have not been previously characterized. [score:1]
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18
[+] score: 4
IL6ST, which is supposed to be up-regulated by decreased levels of has-miR-130b-3p and has-miR-505-3p, encodes glycoprotein 130 (gp130) [60]. [score:4]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-212, hsa-mir-132, hsa-mir-146a, hsa-mir-155, hsa-mir-330
do) which identified miR-132/212 being able to target both IL-1α and IL-1β [IL-1α: miR-330-5p, 326, 211, 204, 488, 185, 328, 149, 299-3p, 495, 590-5p, 21, 132, 212, 340 and 144; IL-1β: miR-505, 200a, 141, 30e, a, d, c, b, 543, 181d, b, c, a, 212, 132, 24, 543, 448, 203, 136, 205, 410, 340, 374a, b, 365, 874, 150, 149, 125a-3p, 590-3p, 140-5p, 494, 194 and 653]. [score:3]
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[+] score: 3
Our results reported 42 differentially expressed miRNAs in PBLs cultured for 24 h in MMG with respect to 1 g, of which 14 (miR-34a-5p, miR-34b-5p, miR-663a, miR-135a-3p, miR-1225-5p, miR-940, miR-221-5p, miR-29b-1-5p, miR-10a-5p, let-7i-3p, miR-200a-3p, miR-7-5p, miR-7-1-3p, and miR-505-5p) were found altered also by γ-irradiation, as assessed in our previous study [47]. [score:3]
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[+] score: 3
Differential expression between good and poor performers (minimum of two-fold difference) was observed for hsa-miR-505, hsa-miR-34a, hsa-miR-1275, hsa-miR-125a-5p, hsa-miR-449a, hsa-miR-155, hsa-miR-101#, hsa-miR-375, hsa-miR-96, hsa-miR-217 and hsa-miR-125b. [score:3]
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[+] score: 3
Next, to further explore the functions of these miRNAs in HCC, we selected miRNAs with a fold change >5, namely hsa-miR-636, hsa-miR-671, hsa-miR-489, hsa-miR-26a, hsa-miR-320, hsa-miR-628, hsa-miR-505, hsa-miR-100, hsa-miR-664, hsa-miR-942, hsa-miR-192, hsa-miR-99b, hsa-miR-125b, hsa-miR-10b, hsa-miR-30b, and hsa-miR-145, for GO (Gene Ontology) enrichment analysis [21] of their target genes using the web -based software WebGestalt 2.0 [22]. [score:3]
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23
[+] score: 3
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-30a, hsa-mir-32, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-30d, hsa-mir-196a-2, hsa-let-7g, hsa-let-7i, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-149, hsa-mir-200c, hsa-mir-425, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-625, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-548e, hsa-mir-548j, 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-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-664a, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-3146, hsa-mir-548v, hsa-mir-3174, hsa-mir-548w, hsa-mir-3192, hsa-mir-548x, hsa-mir-3605, hsa-mir-3662, hsa-mir-548y, 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-664b, 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
In addition, we found three miRNA*s (miR-664*, miR-505* and miR-32*) that were differentially expressed between the two cell types with at least a 5x fold change. [score:3]
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[+] score: 3
34 hsa-miR-335 −0.35hsa-miR-345 [44], [53], [71] 1.16 hsa-miR-363 0.99 hsa-miR-371-5p 0.55 hsa-miR-421 0.50 hsa-miR-483-5p 1.33 hsa-miR-494 0.87 hsa-miR-505* −0.40 hsa-miR-513a-5p 1.06 hsa-miR-513b 1.19 hsa-miR-513c 1.22 hsa-miR-551b −0.40 hsa-miR-574-5p 0.97hsa-miR-630 [68], [73] 0.96 hsa-miR-769-5p −0.34 hsa-miR-801 0.66 hsa-miR-873 −0.64 hsa-miR-877* 0.72 hsa-miR-923 0.89 hsa-miR-940 0.49 hsa-miR-95 −0.44 hsa-miR-99a −0.64Irradiated and non-irradiated PBL of the same donors were incubated in static gravity (1 g) for 4 and 24 h, and miRNA expression profile was analyzed at the end of each incubation time. [score:3]
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25
[+] score: 3
Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, 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-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, 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-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, 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-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
In the miR-28 network (Figure 8C), ASF/SF2 expression is modulated by miR-28 and miR-505 (not show here) which are negatively controlled by LRF to influence the proliferation and survival of mouse embryonic fibroblasts [75]. [score:3]
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26
[+] 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-139, 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, 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]
27
[+] score: 2
Pre-clinical studies in healthy mice and in vitro studies using estrogen have identified miRNAs either regulated by estrogen (miR-203, miR-126, miR-23a, miR-21, miR-24, miR-27a and b, and miR-106a and b) or encoded by X-chromosome (miR-98, miR-652, miR-221, miR-222, miR-223, miR-361, miR-421, miR-325, miR-188, miR-92a, miR-424, miR-503, miR-505). [score:2]
[1 to 20 of 1 sentences]
28
[+] score: 2
The miRNAs differentially regulated by prenatal stress includes miR-23a (up), miR-129-2 (up), miR-361 (down), let-7f (up), miR-17-5p (down), miR-98 (up), miR-425 (down), miR-345-5p (down), miR-9 (up), miR216-5p (up), miR-667 (up), and miR-505 (down) (Figure 3A). [score:2]
[1 to 20 of 1 sentences]
29
[+] score: 1
Indeed, some miRNAs that have been previously linked to carcinogenesis of different organs and tissues, such as miR-2861 [47, 48], miR-4530 [49], miR-638 [50], miR-371b-5p [51], miR-1225-5p [52, 53], miR-296-5p [54, 55], miR-4787-5p [56], miR-4281 [57], miR-4455 [58], miR-197-3p [59], miR-369-5p [60, 61] and miR-505-3p [62] which were found to be altered in brucellosis in our analysis. [score:1]
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30
[+] score: 1
crescentic IgA-GN as well as miR-30c-5p, miR-30b-5p, hsa-miR-505-5p in controls vs. [score:1]
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31
[+] score: 1
Other miRNAs from this paper: hsa-mir-28
A recent study shows that LRF represses the microRNAs miR-28 and miR-505 [22]. [score:1]
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32
[+] score: 1
Interestingly, mRNAs correlated with four core response miRNAsmiR-155–5p, miR-505–3p, miR-7-5p and miR-940 – showed an enrichment in innate immune functions (e. g. innate immune response, immune system process and response to bacterium) [55]. [score:1]
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33
[+] score: 1
We found that some genes, including ALDH3A, JAK2 and miR-505, showed a decreased level of DNA methylation in IHCC organoids that had been cultured in DM, whereas genes that are associated with hepatocyte differentiation showed no significant difference in DNA methylation. [score:1]
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