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40 publications mentioning hsa-mir-625

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-625. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 308
The MAPK kinase MAP2K6 is a direct target of miR-625-3pTo identify miR-625-3p target genes, we searched the transcriptional profile for mRNAs with miR-625-3p target sequences that were downregulated in the SW620.625 cells. [score:11]
Ectopic expression of miR-625-3p promotes oxPt resistanceWe constructed a Sleeping Beauty (SB) transposon vector (pSBInducer), which allows for stable expression of small interfering RNAs (siRNAs) and miRNAs in a DOX-inducible manner (Supplementary Fig. 1), and consequently, robust downregulation of targeted genes in mammalian cells (Supplementary Fig. 2). [score:10]
We selected the eight most downregulated genes with a miR-625-3p target sequence and a miRmap score above 75: MAP2K6, RCN1, BCL11A, COMMD8, MXI1, NUP35, ST18 and IRAK2 (Supplementary Table 2), and confirmed downregulation of these genes by quantitative real-time PCR (Supplementary Fig. 5). [score:9]
To identify miR-625-3p target genes, we searched the transcriptional profile for mRNAs with miR-625-3p target sequences that were downregulated in the SW620.625 cells. [score:8]
In both cell lines miR-625-3p induction increased oxPt resistance over a range of concentrations (Fig. 1b), which translated into an increase in the half maximum inhibitory concentration IC [50] (causing 50% inhibition of viability) from 1.6 μM in HCT116. [score:7]
In total, 216 and 163 genes were up- and downregulated, respectively, in miR-625-3p expressing SW620.625 cells (absolute fold change >1.5; ). [score:6]
To further corroborate the importance of MAP2K6 for mediating the effect of miR-625-3p in CRC cells, we generated stable HCT116 cell lines expressing a dominant -negative version of MAP2K6 harbouring a K82A mutation, which abolishes kinase activity 16. showed the dominant -negative MAP2K6 to be expressed at many times higher level than the endogenous MAP2K6 (Fig. 5e). [score:6]
Up- and downregulated genes after miR-625-3p induction in SW620 cells Proteins dysregulated after miR-625-3p induction in HCT116 cells Oligos used (a) Cell proliferation upon DOX induction of miR-625-3p in the CRC cell lines HCT116.625, SW620.625 and control cells expressing a scrambled shRNA was determined by an MTT assay after 72 h of growth. [score:6]
Overall, we found enrichment for mRNAs containing the miR-625-3p 7-mer target sequence (CTATAGT) in their 3′UTR among downregulated genes (Fig. 4a). [score:6]
In conclusion, we have shown that overexpression of miR-625-3p in CRC cells can induce resistance to oxPt by directly targeting MAP2K6 and consequently inactivating genotoxic stress signalling conveyed by the MAP2K6–MAPK14 pathway. [score:6]
Taken together, these data show that inhibition of MAPK14 phenocopies the effect of miR-625-3p overexpression and supports the notion that the MAP2K6–MAPK14 signalling network plays a central functional role in miR-625-3p -induced oxPt resistance (Fig. 7h). [score:5]
We used pSBInducer to introduce miR-625-3p expression (or control shRNA designed not to target any human transcripts) in the microsatellite stable and microsatellite instable CRC cell lines SW620 and HCT116, respectively (Supplementary Fig. 1). [score:5]
Note that for clarity, the log [2](625/ctrl)-scale is truncated at −1 and 1. (b) The 625/ctrl -expression ratios of eight candidate target genes were determined by qRT–PCR after induction of miR-625-3p (or control) in SW620 cells and HCT116 CRC cells. [score:5]
To identify putative miR-625-3p target genes, 3′UTR sequences were obtained from TargetScan (6.2) for all human annotated transcripts, and the longest 3′UTR sequence was chosen for isoforms with identical gene symbol. [score:5]
Up- and downregulated genes after miR-625-3p induction in SW620 cells Proteins dysregulated after miR-625-3p induction in HCT116 cells Oligos used Supplementary Figures 1-16, Supplementary Tables 1-2 and Supplementary References. [score:5]
The findings reported suggest that the expression level of miR-625-3p, possibly in combination with the expression level and activity of MAP2K6 and MAPK14, has the potential to serve as a biomarker for predicting response to oxPt. [score:5]
To the best of our knowledge, MAP2K6 is the first functionally documented target of miR-625-3p, and conversely, miR-625-3p is the first described microRNA targeting MAP2K6. [score:5]
In conclusion, our data demonstrate that ectopic expression of miR-625-3p promotes resistance towards oxPt in CRC cells, and that this resistance is caused, at least in part, by inhibition of oxPt -induced cell death. [score:5]
MAP2K6 is a direct and functional target of miR-625-3p. [score:4]
It is likely that miR-625-3p additionally could mediate resistance by regulating other unknown target proteins. [score:4]
Increased miR-625-3p expression reduces oxPt -induced cell deathTo determine whether inhibition of cell death was a contributing factor to the observed oxPt resistance in HCT116.625 and SW620.625 cells, we performed a lactate dehydrogenase activity (LDH) assay. [score:4]
This line represents a tumour etiology distinct from HCT116 and SW620 by being microsatellite stable, expressing a truncated TP53 variant, and displaying a hypermutator phenotype as a consequence of a POLE missense mutation 23. miR-625-3p levels in HCC2998.625 cells after DOX induction was increased >20-fold (Supplementary Fig. 10) and associated with decreased MAP2K6 levels as well as with decreased MAPK14 activity (Fig. 7d). [score:4]
The MAPK kinase MAP2K6 is a direct target of miR-625-3p. [score:4]
The presented results are consistent with a mo del were miR-625-3p through downregulation of MAP2K6 impairs p38-MAPK stress signalling (Fig. 7h and Supplementary Fig. 15c). [score:4]
Anti-miR treatment also increased the sensitivity of control cells toward oxPt, although the difference was only borderline significant (P=0.140, t-test), presumably reflecting an effect of downregulating the endogenous miR-625-3p (Fig. 2c). [score:4]
Dominant -negative MAP2K6 expressing cells showed a ∼40% reduction in 64 μM oxPt -induced cell death compared with control HCT116 cells (Fig. 5e), and hence, mimics the phenotype of miR-625-3p overexpressing cells. [score:4]
At the protein level, however, only MAP2K6 were robustly downregulated after miR-625-3p induction in SW620.625 cells (Fig. 4d and Supplementary Fig. 6). [score:4]
Since MAP2K6 levels in HCT116 cells approached the detection limit of western blotting (Supplementary Fig. 7), we estimated miR-625-3p -associated MAP2K6 reduction by mass spectrometry quantification, which showed a mean downregulation of 3.6- and 1.7-fold in SW620.625 and HCT116.625, respectively (Fig. 4e). [score:4]
Altogether, the data strongly support that MAP2K6 is a direct and functional target of miR-625-3p. [score:4]
How to cite this article: Rasmussen, M. H. et al. miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signalling in human colorectal adenocarcinoma cells. [score:4]
Altogether, these data suggest that the oxPt-resistant phenotype induced by miR-625-3p in CRC cells operates through the direct target MAP2K6. [score:4]
On the basis of our results using chemical inhibitors and MAPK14 knockdown, and in agreement with other studies 38 39, we are inclined to believe that the MAPK14 isoform of p38 is a mediator of miR-625-3p -induced oxPt resistance. [score:4]
Increased miR-625-3p expression reduces oxPt -induced cell death. [score:3]
The latter in agreement with the notion that miR-625-3p targets MAP2K6. [score:3]
We used western blotting and quantitative PCR with reverse transcription (qRT–PCR) to confirm expression of FLAG-MAP2K6 protein and miR-625-3p, respectively. [score:3]
Genes were ranked by fold change in expression between miR-625-3p induction and scrambled control. [score:3]
A small decrease in cell death was also observed for 2 and 8 μM oxPt in miR-625-3p overexpressing SW620.625 cells although this was only borderline significant (Fig. 2a). [score:3]
We next investigated how ectopic expression of the miR-625-3p insensitive MAP2K6 variant affected the ability of miR-625-3p to inhibit oxPt -induced cell death (Fig. 5d). [score:3]
Taken together, these findings indicate that increased oxPt resistance mediated by miR-625-3p is conveyed through its target MAP2K6. [score:3]
Speculating whether the observations could be generalized and extended to additional CRC cell lines we generated stable, inducible miR-625-3p expression in the HCC2998 CRC cell line (Fig. 7d). [score:3]
Induction of miR-625-3p in HCT116.625 cells inhibited drug -induced cell death when exposed to oxPt (Fig. 2a). [score:3]
Previously, we reported that high expression of miR-625-3p in primary tumours of mCRC patients was associated with an odds ratio above 6 for a poor response to first-line oxPt -based therapy 5. In the present work, we have shown that miR-625-3p functionally leads to oxPt resistance by preventing the DNA damage response system to induce cell cycle arrest and apoptosis. [score:3]
miR-625-3p inhibits oxPt -induced cell death in CRC cell lines. [score:3]
Indeed, although not reaching significance, we found that MAP2K6 was negatively correlated with miR-625-3p expression in 26 mCRC tumours (Pearson's r=−0.22; Fig. 5f). [score:3]
Furthermore, we have identified MAP2K6 as a functional target for miR-625-3p, and as a mediator of miR-625-3p -induced oxPt resistance. [score:3]
The close-up depicts miR-625-3p annealed to the wild-type target sequence (underlined) as well as the two mutated sequences used in g. (g) Mean normalized Renilla Luc signal±s. [score:3]
Increased CDK activity at the G1/S checkpoint or in early M phase was also indicated by S138/S151 phosphorylations on inactivated FZR1 (also known as CDH1) in miR-625-3p expressing cells, whereas unphosphorylated FZR1 in control cells suggested decreased CDK signalling at G0 or early G1 (ref. [score:3]
Supplementary Data 1. Supplementary Data 2. Supplementary Data 3. Ectopic expression of miR-625-3p is associated with increased viability in oxPt medium. [score:3]
Collectively, this indicates that miR-625-3p overexpression leads to decreased activity of MTOR, MAPK1 and the MAPK14 kinases. [score:3]
For anti-miR experiments, cells were DOX -induced for 24 h prior transfection with anti-miR (MH12612, mirVana miRNA inhibitor (miRBase ID: hsa-miR-625-3p) catalogue (Cat. ) [score:3]
org/app/) 8 was used with standard parameters using the options ‘Species'=Human and ‘miRNA'=hsa-miR-625-3p; Candidate target genes with a miRmap score >75 were extracted. [score:3]
In addition, the observation that anti-miR-625-3p treatment makes cells with high miR-625-3p level responsive to oxPt, indicates that it may be possible to sensitize patients with high miR-625-3p expressing cancers to oxPt by miR-625-3p antagonist treatment before, or simultaneously with, oxPt treatment. [score:3]
These data indicate a clinical relevance for the oxPt-resistant phenotype induced by ectopic miR-625-3p overexpression. [score:3]
Similar to HCT116 and SW620 cells, ectopic miR-625-3p expression reduced the 64 μM oxPt -induced cell death to ∼75% of control cells (Fig. 7e). [score:3]
Ectopic expression of miR-625-3p had no significant effect on cell growth in SW620 cells, whereas in HCT116 cells, a slight (28%) increased viability was observed (Fig. 1a). [score:3]
Forty-eight hours of DOX induction raised the level of miR-625-3p approximately three-fold in HCT116.625 cells, which is comparable to the previously reported difference in miR-625-3p expression between responder and non-responder patients (Supplementary Fig. 3) 5. In SW620.625 cells, DOX treatment induced miR-625-3p by more than 400 fold (Supplementary Fig. 3). [score:3]
In contrast, increased S130 phosphorylation was seen in cells with ectopic miR-625-3p expression. [score:3]
Since up to 20% of mCRC patients show high miR-625-3p expression 5, the number of patients that potentially could benefit from quantification of the miR-625-3p biomarker is substantial. [score:3]
Ectopic expression of miR-625-3p promotes oxPt resistance. [score:3]
In support of miR-625-3p regulating MAP2K6 signalling, we observed reduced phosphorylation of MAPK14 [Tyr180/Y182] upon miR-625-3p-induction (Fig. 5a). [score:2]
miR-625-3p dysregulates MAPK signalling pathways. [score:2]
In contrast, the oxPt response in the context of miR-625-3p led to increased pS/pTP-R/K -associated kinase activity, and generally, decreased R-pS-directed activity, while phosphorylations on pS/pTP motifs, in general, were similar in ctrl and 625 cells (Fig. 9c). [score:2]
miR-625-3p regulates resistance to oxPt through MAP2K6 and MAPK14. [score:2]
miR-625-3p dysregulates MAPK signalling pathwaysThe results presented above indicates that the p38 MAPK subfamily (MAPK11–14) could be implicated as a mediator of platinum drug -induced stress signalling including apoptosis, a concept that has been exploited by others 17 18. [score:2]
Furthermore, specific mutation of the miR-625-3p seed sequence (3′UTR mut1 and mut2) completely abolished miR-625-3p -mediated reduction of Luc (Fig. 4g). [score:2]
When transfected into HEK293T cells together with pre-miR-625-3p, Luc expression was reduced with 75% as compared with mock transfected cells (that is, Luc reporter with no MAP2K6 3′UTR) (Fig. 4g). [score:2]
miR-625-3p blocks the normal cellular response to oxPtWe next investigated whether miR-625-3p expression affected the predicted activities of the oxPt-regulated kinases identified by KSEA (see Fig. 8d,e). [score:2]
miR-625-3p regulates networks associated with therapy response. [score:2]
We reasoned that a stronger impact on target mRNAs would be seen in SW620.625 cells as compared with HCT116.625 cells owing to the higher miR-625-3p levels in the former (Supplementary Fig. 3). [score:2]
We next investigated whether miR-625-3p expression affected the predicted activities of the oxPt-regulated kinases identified by KSEA (see Fig. 8d,e). [score:2]
Wild-type and mutated versions of part of the MAP2K6 3′UTR centred on the miR-625-3p target site were generated by primer extension PCR using oligos notI-map2k6.3UTR-rev and either of xhoI-map2k6.3UTR. [score:2]
shRNA DNA (siR [EGFP], miR-625-3p or scramble) and 1,500 ng pCMV-SB100XCO helper plasmid (or, as a negative control, 1,500 ng pUC19 DNA) using 15 μl Lipofectamine 2000 (Invitrogen) in 500 μl Opti-Mem I Medium (Gibco, Invitrogen-Life Technologies). [score:1]
To mechanistically investigate the role of MAP2K6 in oxPt response in CRC cells, we stably expressed MAP2K6 lacking the miR-625-3p binding site in HCT116.625 cells. [score:1]
This suggests that miR-625-3p acts after, or independently of, the immediate ATM/ATR -mediated DNA damage response (Supplementary Fig. 15c). [score:1]
However, when cells with increased miR-625-3p levels (HCT116.625. [score:1]
Critical components of the cellular response to oxPt are blocked in cells with increased miR-625-3p levels. [score:1]
Altogether, these analyses are in support of the hypothesis that miR-625-3p induces blockage of signalling pathways involved in normal oxPt response, which, among other things, culminates in increased cell cycle progression signals relative to control cells. [score:1]
To investigate whether sensitivity towards oxPt could be restored by reducing miR-625-3p levels, the most oxPt-resistant HCT116.625 clone (clone #1) was transfected with an inhibitor of miR-625-3p (an anti-miR). [score:1]
We observed resistance to oxPt after miR-625-3p induction in all three cell mo dels—with the strongest phenotype obtained in HCT116 cells—despite different levels of induction (3 × in HCT116, 25 × in HCC2998 and >400 × in SW620) and different degrees of MAP2K6 reduction (0.8 × in HCT116, 0.4 × in HCC2998 and 0.2 × in SW620). [score:1]
This indicates that the resulting level of MAP2K6 protein—rather than changes in miR-625-3p and MAP2K6 per se—determines response to oxPt. [score:1]
The MAP2K6 3′UTR contains a putative 8mer miR-625-3p seed site with a miRmap score of 85.49 (Fig. 4f). [score:1]
Experiments where a miR-625-3p or control (Scr) pre-miR were co -transfected together with psiCHECK-2 are indicated. [score:1]
It is important to emphasize, however, that our mo del only addresses miR-625-3p signalling through MAP2K6. [score:1]
miR-625-3p luciferase reporter assayWild-type and mutated versions of part of the MAP2K6 3′UTR centred on the miR-625-3p target site were generated by primer extension PCR using oligos notI-map2k6.3UTR-rev and either of xhoI-map2k6.3UTR. [score:1]
This indicates that miR-625-3p functionally is associated with increased resistance to oxPt in CRC cells. [score:1]
In support of mitotic -induced nuclear lamina breakdown, increased phosphorylation was observed on multiple residues on LMNA in miR-625-3p cells; On the contrary, these became dephosphorylated after oxPt treatment in control cells indicating decreased cell cycle progression (also see Supplementary Fig. 14). [score:1]
In the 625+OX/ctrl+OX experiment, a mean log [2] ratio different from zero is expected for kinases whose activities after oxPt treatment are altered by increased miR-625-3p levels, while unaffected kinases will have a mean log [2] ratio around zero. [score:1]
In agreement with the miR-625-3p -induced oxPt resistance phenotype (Fig. 2a,b), this suggested that miR-625-3p blocks signalling cascades central in the normal response to DNA damage. [score:1]
miR-625-3p transcripts are associated with oxPt response. [score:1]
We first looked at the overall effect on the phosphoproteome after 48 h of increased miR-625-3p levels. [score:1]
We finally asked whether MAP2K6 might be correlated with miR-625-3p and chemotherapy response in patients? [score:1]
Following this, CRC patients with high mir-625-3p levels and reduced MAP2K6–MAPK14 signalling, and therefore resistance to oxPt, may instead benefit from irinotecan treatment as first-line therapy. [score:1]
miR-625-3p transcripts are associated with oxPt responseTo identify genes associated with the oxPt-resistant phenotype, transcriptional profiles of DOX -induced SW620.625 and SW620. [score:1]
The reduction was specifically related to miR-625-3p since co-transfection with a control pre-miR (Scr) had no effect on Luc (Fig. 4g). [score:1]
The cumulative distribution of genes with a miR-625-3p seed sequence (red) was significantly different from the distribution of genes without a seed sequence (black) (P=1.9*10 [−5], Kolmogorov–Smirnov test; top panel). [score:1]
Our phosphoproteome data in exponentially growing unstressed CRC cells also revealed that MAPK14 was the kinase whose activity (on a substrate level) was mostly affected by miR-625-3p induction. [score:1]
The miR-625-3p specific pS/pTP-R/K motif was most strongly associated with cyclin -dependent kinases (CDK1, CDK2 and CDK5), and to a lesser extent with MAP kinases and TTK kinase. [score:1]
Western blot against MAP2K6 (f) Correlation between MAP2K6 mRNA levels and mir-625-3p in clinical samples (P=0.212, Pearson's correlation). [score:1]
miR-625-3p blocks the normal cellular response to oxPt. [score:1]
The percentage of apoptotic cells in non -treated cells was similar in control and miR-625-3p cell clones, while the death rate upon exposure to oxPt was reduced from 81% in control cells to below 50% in the HCT116.625 cell clones. [score:1]
ctrl cells were induced with DOX and transfected with 20 nM anti-miR-625-3p oligo. [score:1]
KSEA indicated decreased activity of MAPK8, MAPK14, MAPK1 and MTOR kinases, and increased activity of the CDK7, PRKACA and CSNK2A1 kinases, respectively, after miR-625-3p induction (Fig. 6c). [score:1]
Decreased MAPK signalling is associated with miR-625-3p induction. [score:1]
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[+] score: 305
The strong association of miR-625-3p expression with high degrees of CD8+ T cell proliferation was further supported by the necessity of repetitive IL-2 supplementation to maintain high miR-625-3p levels and the lack of significant miR-625-3p upregulation upon withdrawal of IL-2. Finally, the mTOR inhibitor rapamycin which inhibits the T cell proliferation by negatively regulating cell cycle proteins and cytokine signaling mechanisms [33– 35] lead to significant inhibition of miR-625-3p upregulation. [score:16]
Overall, these data suggest that although TCR stimulation upregulates miR-625-3p expression, maintenance of elevated miR-625-3p expression is dependent on the ongoing T cell proliferation. [score:8]
[31, 32] Our studies on miR-625-3p expression in relation to other cellular functions after TCR dependent T cell stimulation revealed that miR-625-3p is upregulated only after first signs of T cell activation, including CD69 (6h) or CD25 and CD71 (1 day) expression on the cell surface, IFN-γ release (3d) and largely parallels the kinetics T cell proliferation. [score:8]
Subsequently, we investigated whether inhibition of proliferation of CD2/CD3/CD28 bead stimulated CD8+ T cells using the mTOR inhibitor rapamycin also inhibits miR-625-3p expression (Fig 3G and 3H). [score:7]
Transfection experiments with miR-625-3p overexpression and silencing systems for e. g. using anti-sense miRNA targeting miR-625-3p are needed to refine the target molecules of miR-625-3p and to elucidate the function of miR-625-3p in human CD8+ T cells. [score:7]
In order to ascertain whether TCR dependency is mandatory for miR-625-3p upregulation, further studies on miR-625-3p expression in human T cells stimulated via TCR independent mechanisms are required such as CD31 triggering or transfection of P2X receptors regulating autocrine T cell activation. [score:7]
Due to the observed close association between miR-625-3p expression and T cell proliferation in vitro, we assumed that miR-625-3p might also be upregulated in CD8+ T cells during strong immune responses such as severe acute GvHD in vivo. [score:6]
Indeed, miR-625-3p expression in CD8+ T cells was highly upregulated shortly after allogeneic SCT when peripheral T cell numbers were still low and declined down to levels comparable to healthy donors in parallel with reaching maximum CD8+ T cell numbers on day 150 post-transplant. [score:6]
Recently, overexpression of miR-625-3p in colorectal cancer cell lines had been shown to provide resistance to apoptosis via downregulating p38-MAPK which is involved in phosphorylation and activation of the pro-apoptotic bcl-2 gene[22]. [score:6]
In conclusion, this study has demonstrated for the first time that the expression of cancer-related miR-625-3p is upregulated in CD8+ T cells in vitro upon TCR mediated activation and is tightly linked to the level of CD8+ T cell proliferation. [score:6]
Accordingly, only stimulation with CD2/CD3/CD28 beads or with PHA +IL-2 resulted in a more than two fold miR-625-3p upregulation, while miR-625-3p expression remained low after stimulation with cytokines or PHA alone (Fig 1B). [score:6]
Inhibition of proliferation in CMV and HA-1 specific CTL clones decreases miR-625-3p upregulation. [score:6]
While BrdU uptake was considerably inhibited (Fig 3G), miR-625-3p expression was almost abrogated by rapamycin (Fig 3H). [score:5]
Thus, miR-625-3p upregulation is a late marker of T cell activation. [score:4]
Therefore, we analyzed whether also antigen-specific stimulation can upregulate miR-625-3p in CD8+ T cells. [score:4]
Due to the similarities in regulative functions in cancer and T-cells previously shown for an increasing number of miRNAs we assumed also a differential expression of miR-625-3p in lymphocytes. [score:4]
Thus, CD8+ T cells proliferation induced by TCR stimulation along with co-stimulation provided by APCs was accompanied by miR-625-3p upregulation. [score:4]
These data suggest that miR-625-3p expression in CD8+ T cells is differentially regulated during distinct phases of CD8+ T cell reconstitution after allogeneic SCT. [score:4]
This lead to the hypothesis that miR-625-3p might also be upregulated in CD8+ T cells during strong immune responses such as severe acute GvHD grade II-IV after allogeneic SCT. [score:4]
Assuming that proliferation in the overall CD8+ T cell compartment is too low during acute GvHD to detect miR-625-3p upregulation in vivo, we investigated miR-625-3p expression during CD8+ T cell reconstitution after allogeneic SCT. [score:4]
Therefore, peripheral blood samples collected on day 45 after allogeneic SCT were used to analyze in all patients whether miR-625-3p expression in CD8+ T cells was dysregulated in patients with acute GvHD grade II-IV within the observation period. [score:4]
Subsequently, we studied the kinetics of miR-625-3p upregulation in parallel to T cell activation and proliferation. [score:4]
Thus, miR-625-3p is detectable only late after upregulation of T cell activation surface markers and associates well with T cell proliferation and IFN-γ release. [score:4]
Thus, the overall CD8+ T cell compartment might not have proliferated sufficiently during GvHD to allow detection of miR-625-3p upregulation. [score:4]
miR-625-3p upregulation in CD8+ T cells is transient and proliferation -dependent. [score:4]
miR-625-3p upregulation in CD8+ T cells after stimulation. [score:4]
Peptide stimulation resulted in a significant peptide dependent BrdU uptake (p = 0.003, p = 0.002, respectively, unpaired t-test, Fig 1C) and more than two fold upregulation of miR-625-3p (Fig 1D). [score:4]
miR-625-3p is upregulated in CD8+ T cells during immune reconstitution after allogeneic SCT. [score:4]
miR-625-3p expression is regulated during CD8+ T cell reconstitution in vivo. [score:4]
miR-625-3p upregulation is a late event after T cell activation. [score:4]
Namely, our in vitro data indicate the importance of TCR stimulation in comparison to only cytokines for the upregulation of miR-625-3p in CD8+ T cells. [score:4]
miR-625-3p is upregulated in proliferating CD8+ T cells after strong TCR stimulation. [score:4]
To the best of our knowledge, the presented analysis is the first study on miRNA expression in isolated human CD8+ T cells after allogeneic SCT and shows that miR-625-3p is highly regulated during CD8 T cell reconstitution. [score:4]
Overall, these data show that strong TCR dependent stimuli either supported by cytokines or co-stimulation induce miR-625-3p upregulation in CD8+ T cells. [score:4]
In conclusion, miR-625-3p expression in CD8+ T cells was not a biomarker of severe acute GvHD in our cohort. [score:3]
Additionally, mHag specific T cells within the CD8+ T cell compartment expanding during GvHD[40] might have been present in too small numbers to influence miR-625-3p expression. [score:3]
Moreover, there were no statistically significant differences in miR-625-3p expression between CD8 T cells derived from patients with or without acute GvHD (p = 0.177, Mann-Whitney U test, Fig 4C). [score:3]
Overexpression of miR-625-3p in CRC cell lines promotes migration and invasion[23]. [score:3]
These data are in accordance with our in vitro data showing a close association between the levels of CD8+ T cell proliferation and of miR-625-3p expression. [score:3]
Of note, this increase of miR-625-3p expression was only present in proliferating CD8+ T cells stimulated via the CD3-TCR complex, i. e. via CD2/CD3/CD28 beads or PHA [25, 27] with IL-2 supplementation. [score:3]
Significant increase in IFN-γ levels (p = 0.037) and miR-625-3p expression (>2 fold change) was observed on day 3 preceding CD8+ T cell proliferation detected by a significant increase in BrdU uptake at day 5 post stimulation (p = 0.005, all paired t-test, Fig 2B–2D). [score:3]
Moreover, miR-625-3p expression in CD8+ T cells was not predictive for severe acute GvHD in patients with acute GvHD. [score:3]
0183828.g002 Fig 2. (A-D) CD8+ T cells isolated from PBMCs of 4 healthy donors were stimulated with PHA + 120 IU/ml IL-2 and (A) CD69, CD25 and CD79 surface expressions, (B) IFN-γ in the supernatant, (C) BrdU uptake and (D) intracellular miR-625-3p expression were measured after 0h, 6h, 1, 3, 5 and 7 days. [score:3]
High expression of miR-625-3p at an early time point during CD8+ T cell expansion after allogeneic SCT suggests that miR-625-3p might be applicable as intracellular biomarker for an effective immune reconstitution. [score:3]
Additional studies are required to identify the targets and function of miR-625-3p in human CD8+ T cells and to confirm the predictive value of miR-625-3p for the speed of CD8+ T cell reconstitution. [score:3]
Thus, high miR-625-3p expression in CD8+ T cells was associated with the rapid increase of CD8+ T cell numbers early after allogeneic SCT and declined with the time post-transplant. [score:3]
Subsequently, we analyzed whether miR-625-3p expression in CD8+ T cells might predict the acute GvHD risk in patients with acute GvHD grade II-IV by comparing the last samples collected before onset of acute GvHD with samples collected during acute GvHD. [score:3]
In order to identify a potential association between miR-625-3p and severe acute GvHD, miR-625-3p expression was analyzed in peripheral blood CD8+ T cells isolated from 137 longitudinally collected peripheral blood samples of 74 patients after allogeneic SCT (Table 1). [score:3]
However, there was no difference in miR-625-3p expression in CD8+ T cells on day 45 after allogeneic SCT in patients with and without severe acute GvHD. [score:3]
Here, we studied for the first time the expression dynamics of miR-625-3p in human CD8+ T cells both in vitro and after allogeneic SCT in vivo. [score:3]
Thus, high miR-625-3p expression might indicate an effective CD8+ T cell reconstitution after allogeneic SCT. [score:3]
miR-625-3p expression in total CD8+ T cells isolated from the peripheral blood of healthy donors was analyzed upon T cell proliferation induced by different stimuli, i. e. CD2/CD3/CD28 beads, the CD3-TCR binding lectin PHA [25, 26] and the cytokines IL-2 or IL-7+IL-15. [score:3]
However, the expression and relevance of miR-625-3p had not been studied in T cells. [score:3]
Subsequently, the relative miR-625-3p expression (black circles) was determined. [score:3]
Subsequently, we studied miR-625-3p expression in CD8+ T cells in relation to the sampling time point post-transplant. [score:3]
In contrast, samples without repetitive addition of IL-2 showed only a transient BrdU uptake (Fig 3D) and increase of cell numbers (Fig 3F) but no significant miR-625-3p expression (Fig 3E). [score:3]
PHA or IL-2 alone or the homeostatic cytokines IL-7 and IL-15 were capable to induce T cell proliferation to a lower extent as known from previous studies[30] but insufficient to induce miR-625-3p expression. [score:3]
In order to investigate the dependency of miR-625-3p expression on ongoing T cell proliferation, we studied the long-term kinetics of BrdU uptake, miR-625-3p expression and live cell counts in CD8+ T cells after PHA + IL-2 stimulation with (Fig 3A–3C) or without (Fig 3D–3F) repeated IL-2 supplementation until day 20 or 17, respectively. [score:3]
The relationship between collection time and miR-625-3p expression in CD8+ T cells was analyzed by Spearman correlation coefficient (R [2]) analysis. [score:3]
However, it remains unclear whether miR-625-3p directly regulates mTOR pathway or has a functional effect on CD8+ T cell proliferation via other pathways that may provide a survival advantage, e. g. apoptosis resistance, cytokine secretion or enhanced TCR signaling. [score:3]
Additionally, miR-625-3p expression might provide insights into the mechanisms during early CD8+ T cell reconstitution. [score:3]
0183828.g004 Fig 4 (A) Viable CD3+CD8+ T cells were isolated by FACS sorting from peripheral blood samples and miR-625-3p expression was determined. [score:3]
miR-625-3p expression in CD8+ T cells in relation to proliferation. [score:3]
In contrast, on day 90 and on day 150, i. e. when CD8+ T cell reconstitution was largely completed, miR-625-3p expression in CD8+ T cells was comparable to healthy donors (Fig 5A). [score:3]
So far, our in vitro data indicate a close association between miR-625-3p expression and T cell proliferation in vitro. [score:3]
So far, our data suggest that miR-625-3p expression is linked to the initiation of T cell proliferation. [score:3]
In our in vitro experiments, miR-625-3p expression in human CD8+ T cells was induced by strong proliferative stimuli that involved triggering of the CD3-TCR complex, i. e. via CD2/CD3/CD28 beads, PHA with IL-2 supplementation or antigen-specific stimulation using peptide loaded APCs. [score:3]
Moreover, miR-625-3p expression in CD8+ T cells did not significantly differ between samples collected before and during severe acute GvHD (p = 0.168, Wilcoxon matched-pairs signed rank test, Fig 4D). [score:3]
Overall, miR-625-3p expression in CD8+ T cells was significantly higher (p = 0.031, Mann-Whitney U test) with high variability in peripheral blood of patients after allogeneic SCT compared to healthy donors (Fig 4B). [score:2]
miR-625-3p is not regulated in peripheral blood CD8+ T cells during acute GvHD. [score:2]
Thus, only conditions leading to strong T cell proliferation in our assay were associated with an increase of miR-625-3p expression. [score:2]
[37, 38] Therefore, we performed our analysis of miR-625-3p in the overall CD8+ T cell population assuming that these may comprise sufficient mHag specific T cells to allow detection of GvHD related miR-625-3p regulation. [score:2]
This suggests that miR-625-3p might play a role downstream of the TCR signaling cascade. [score:1]
miR-625-3p levels in CD8+ T cells were significantly and negatively correlated with the time of sample collection after allogeneic SCT (p<0.0001, Spearman R [2] = 0.2) (Fig 5B). [score:1]
We stimulated CD8+ T cells with PHA, supplemented with IL-2 every two days and measured the surface expression of the activation markers CD69, CD25 and CD71; IFN-γ in the supernatant; BrdU uptake and intracellular miR-625-3p after 0h, 6h, 1, 3, 5 and 7 days after stimulation. [score:1]
Left Y-axis: Mean relative miR-625-3p expression calculated by miR-625-3p [RQ]/mean RNU48/U6 snRNA [RQ]. [score:1]
Therefore, we quantified miR-625-3p levels in CD8+ T cells on days 25, 45, 90 and 150 after allogeneic SCT in relation to CD8 T cell counts in the peripheral blood at the respective time points. [score:1]
On day 25 and on day 45, i. e. during rapid CD8+ T cell reconstitution after allogeneic SCT, miR-625-3p expression in CD8+ T cells was significantly higher than in healthy individuals who are characterized by a homeostasis in T cell numbers (p = 0.0015, p = 0.0077, respectively, Mann-Whitney U test). [score:1]
Samples with repetitive IL-2 supplementation showed a persistent increase of BrdU uptake (Fig 3A), miR-625-3p (Fig 3B) and cell numbers (Fig 3C). [score:1]
Statistical comparisons was calculated in comparison with the miR-625-3p expression in CD8+ T cells of healthy donors by Mann-Whitney U test; *indicates p<0.05. [score:1]
BrdU uptake (G) and miR-625-3p expression (H) were measured on day 5 after stimulation. [score:1]
Thus, miR-625-3p is strongly dependent on the continuous provision of a proliferative stimulus. [score:1]
BrdU uptake (A, D), miR-625-3p expression (B, E) and viable cell counts determined by trypan blue staining (C, F) were measured on different days until day 20 (A-C) or 17 (D-F) after stimulation. [score:1]
[22, 23] Moreover, miR-625-3p has been detected in the circulation of malignant pleural mesothelioma patients. [score:1]
miR-625-3p in CD8+ T cells in patients with GvHD. [score:1]
Relative miR-625-3p expression in individual patient samples calculated by miR-625-3p [RQ]/mean RNU48/U6 snRNA [RQ]. [score:1]
BrdU uptake (A) and miR-625-3p expression (B) were measured 5 days after stimulation. [score:1]
In this study, we show for the first time the association of the cancer-related miR-625-3p with human and proliferation in vitro. [score:1]
Recently, abnormal expression of the less characterized miR-625-3p has been described in primary colorectal carcinoma (CRC) and in CRC cell lines. [score:1]
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To this end, we found for the first time that miR-625-3p markedly inhibited SCAI expression and subsequently suppressed E-cadherin and upregulated MMP-9 expression, leading to enhanced cell invasion in CRC (Figure 6). [score:12]
Figure 6 MiR-625-3p inhibited SCAI expression and subsequently suppressed E-cadherin and upregulated MMP-9 expression, leading to enhanced cell migration, invasion and metastasis in CRC. [score:11]
MiR-625-3p inhibited SCAI expression and subsequently suppressed E-cadherin and upregulated MMP-9 expression, leading to enhanced cell migration, invasion and metastasis in CRC. [score:11]
We observed that depletion of miR-625-3p upregulated SCAI and E-cadherin expressions, but down-regulated MMP-9 level in SW620 cells (Figure 5A-5C). [score:9]
Up-regulation of miR-625-3p promoted cell motility, while down-regulation of miR-625-3p inhibited cell invasive activity in CRC cells. [score:9]
Over -expression of miR-625-3p inhibited SCAI expression in SW480. [score:7]
We further explored whether miR-625-3p exerts its oncogenic function via inhibiting its target SCAI (suppressor of cancer cell invasion). [score:7]
We observed that MMP-9 expression was upregulated in SW480 cells after miR-625-3p mimics treatment (Figure 4B, 4C). [score:6]
Down-regulation of miR-625-3p inhibited cell migration and invasion in SW620 cells. [score:6]
Another study showed that miR-625-3p was up-regulated in oxaliplatin resistant CRC cell lines, suggesting that strong expression of miR-625-3p is positively correlated with a poor response to first-line oxaliplatin treatment of metastatic CRC [29]. [score:6]
Down-regulation of miR-625-3p increased SCAI expression. [score:6]
SW620 cells were transfected with miR-625-3p inhibitor (anti-miR-625-3p, Invitrogen) or inhibitor NC (anti-miR-control, Invitrogen) using the Lipofectamine 2000 reagent. [score:5]
Our findings demonstrated that miR-625-3p could promote cell migration and invasion through inhibition of SCAI and its target E-cadherin. [score:5]
As illustrated in Figure 2A, our real-time RT-PCR confirmed that miR-625-3p inhibitors significantly decreased the expression of miR-625-3p in SW620 cells. [score:5]
We found that overexpression of miR-625-3p significantly reduced the SCAI expression at mRNA and protein levels in SW480 cells (Figure 4A, 4B). [score:5]
Due to that E-cadherin and MMP-9 play a critical role in controlling migration and invasion, miR-625-3p could inhibit SCAI and subsequently govern E-cadherin and MMP-9 expression, leading to enhanced invasion in CRC cells. [score:5]
D. Quantitative results are illustrated for panel C. To address whether SCAI is a target of miR-625-3p, we detected the expression of SCAI in SW480 cells transfected with miR-625-3p mimics by real-time RT-PCR and. [score:5]
SW480 cells were chosen for further exploring the function of miR-625-3p through overexpressing strategy by its mimics due to that SW480 cells showed lowest expression of miR-625-3p. [score:5]
A. Real-time RT-PCR was performed to detect the expression of SCAI, MMP-9, and E-cadherin at the mRNA levels in SW620 treated with miR-625-3p inhibitor. [score:5]
Overexpression of miR-625-3p did not increase the cell proliferation at 24 hours (data not shown), suggesting that miR-625-3p governed the cell invasive activity not due to regulation of cell proliferation. [score:4]
In summary, our findings reveal the critical role of miR-625-3p in cell invasion and indicate that downregulation of miR-625-3p may be a promising novel approach for the treatment of CRC. [score:4]
Moreover, downregulation of miR-625-3p retarded the cell motility (Figure 2B, 2C). [score:4]
Consistently, upregulation of miR-625-3p was observed in tumor specimens from malignant mesothelioma patients [30]. [score:4]
B. was performed to detect the expression of SCAI, E-cadherin, and MMP-9 in SW480 cells transfected with miR-625-3p mimic (left panel). [score:3]
Strikingly, we identified SCAI as a potential target of miR-625-3p. [score:3]
Therefore, in the current study, we investigated whether miR-625-3p plays an important role in controlling cancer cell migration and invasion in CRC by overexpression or depletion of miR-625-3p expression in CRC cells. [score:3]
D. Quantitative results are illustrated for panel C. A. SCAI sequence analysis indicates that it harbors potential miR-625-3p target sites, which are nt 6845–6852 sequences of the SCAI 3′ UTR. [score:3]
Here, our data suggest that miR-625-3p inhibited SCAI and led to increased migration and invasion in CRC cells. [score:3]
Inhibition of miR-625-3p reduced cell motility and invasion. [score:3]
The expression of miR-625-3p, SCAI and E-cadherin was correlated in CRC cells. [score:3]
C. Quantitative results are illustrated for panel B. Anti-miR-625-3p: miR-625-3p inhibitor. [score:3]
Our study thus offers a new strategy to treat CRC through inhibiting miR-625-3p level. [score:3]
The results showed that miR-625-3p was frequently but differentially expressed in different human colorectal cancer cell lines (Figure 1A). [score:3]
To further validate the role of miR-625-3p in CRC cells, SW620 cells with highest expression of miR-625-3p were used. [score:3]
A. miR-625-3p level was determined by real-time RT-PCR in SW620 cells with miR-625-3p inhibitor treatment. [score:3]
Cells were transfected with the miR-625-3p mimic or inhibitor when they reached 90% confluence. [score:3]
Consistent with this, high expression of miR-625-3p has also been associated with poor response to first-line oxaliplatin -based treatment for metastatic colorectal cancer [29]. [score:3]
miR-625-3p expression is associated with invasive activity in CRC cell lines. [score:3]
B. was used to measure the expression of SCAI, E-cadherin, and MMP-9 in SW620 cells with miR-625-3p inhibitor treatment (left panel). [score:3]
To further understand the molecular mechanism of miR-625-3p -mediated invasion in CRC cells, we sought to identify the target of miR-625-3p. [score:3]
Over -expression of miR-625-3p promoted cell migration and invasion. [score:3]
Consistent with this, overexpression of miR-625-3p enhanced the migration and invasion in SW480 cells (Figure 1C, 1D). [score:3]
SCAI is a potential downstream target of miR-625-3p. [score:3]
A. Real-time RT-PCR was conducted to detect the expression of SCAI, E-cadherin, and MMP-9 at the mRNA levels in SW480 cells transfected with miR-625-3p mimic. [score:3]
Figure 5Anti-miR-625-3p: miR-625-3p inhibitor. [score:3]
Specifically, we observed the higher expression of miR-625-3p in SW620, HCT116, and Colo205 cells (Figure 1A). [score:3]
SCAI sequence analysis revealed that it harbors potential miR-625-3p target sites, which are nt 6845–6852 sequences of the SCAI 3′ UTR (Figure 3A). [score:3]
Figure 3 A. SCAI sequence analysis indicates that it harbors potential miR-625-3p target sites, which are nt 6845–6852 sequences of the SCAI 3′ UTR. [score:3]
Figure 2Anti-miR-625-3p: miR-625-3p inhibitor. [score:3]
Anti-miR-625-3p: miR-625-3p inhibitor. [score:3]
Accumulating evidence has demonstrated that miR-625-3p is highly expressed in human cancers [29, 30]. [score:3]
A recent series of studies demonstrated that miR-625-3p, one member of miR-625 family, contributed to tumor development, progression and metastasis in malignant mesothelioma and CRC [29, 30]. [score:2]
Notably, we have evidenced that miR-625-3p exerts its oncogenic function in enhancing cell invasion via regulation of SCAI/E-cadherin/MMP-9 pathways. [score:2]
C. Quantitative results are illustrated for panel B. To further verify whether miR-625-3p regulates SCAI/E-cadherin/MMP-9 pathway in CRC cells, we used and RT-PCR to measure SCAI, E-cadherin, and MMP-9 levels in SW620 cells after miR-625-3p inhibitor treatment. [score:2]
Therefore, miR-625-3p -mediated CRC cell migration and invasion may be partly through regulating SCAI/E-cadherin/MMP-9 pathway in CRC. [score:2]
Consistent with this notion, we found that miR-625-3p expression was higher in SW620 and Colo205 cells compared with that of other three cell lines (Figure 1A). [score:2]
Moreover, SW620 cells treated with miR-625-3p inhibitor showed a low level of penetration through the matrigel-coated membrance compared with the control cells (Figure 2D). [score:2]
These data suggest that miR-625-3p could be involved in regulation of invasion in CRC cells. [score:2]
These results suggested that miR-625-3p regulated migration and invasion at least in part through SCAI/E-cadherin/MMP-9 pathway. [score:2]
The level of miR-625-3p was detected using real-time RT-PCR in miR-625-3p mimic transfected cells. [score:1]
Moreover, E-cadherin mRNA and protein levels were also decreased in SW480 cells transfected with miR-625-3p mimics (Figure 4A–4C). [score:1]
Importantly, increased circulating miR-625-3p could be a potential biomarker for patients with malignant pleural mesothelioma (MM) [30]. [score:1]
The RT-PCR was performed according to miR-625-3p qPCR Quantitation Kit (Takara, Kyoto, Japan). [score:1]
To this end, our present study identified that higher expression of miR-625-3p was found in CRC cell lines with poor differentiation, high invasive activity and metastasis characteristics. [score:1]
For instance, miR-625-3p was present in significantly higher concentration in plasma/serum from malignant mesothelioma patients, which can discriminate between patients and control group [30]. [score:1]
Consistent with this, our results support that miR-625-3p controls cell migration and invasion in CRC cells. [score:1]
Moreover, our findings revealed that miR-625-3p enhanced cell migration and invasion in CRC cells. [score:1]
C. Quantitative results are illustrated for panel B. In the current study, we explored the molecular mechanism of miR-625-3p-meidated tumorigenesis in CRC cells. [score:1]
NC: negative control; miR-625-3p: miR-625-3p mimic. [score:1]
Our results showed that miR-625-3p was markedly increased by its mimics treatment (Figure 1A). [score:1]
Taken together, our findings demonstrated that miR-625-3p is involved in promoting cell migration and invasion in CRC cells. [score:1]
A schematic illustration of the signaling network showing how miR-625-3p promotes cell migration and invasion. [score:1]
This study indicated that miR-625-3p could be a novel diagnostic marker for malignant mesothelioma. [score:1]
Our data demonstrated that miR-625-3p level is associated with invasive activity in CRC cell lines. [score:1]
Altogether, miR-625-3p plays a key role in governing cell migration and invasion. [score:1]
C. Quantitative results are illustrated for panel B. To better understand the association between miR-625-3p and cell invasion, the baseline expression of miR-625-3p was measured in a panel of human colorectal cancer cell lines that included SW480, SW620, HT29, HCT116, and Colo205. [score:1]
As E-cadherin is an important factor for cell invasion, miR-625-3p promoted cell invasion partly via modulating SCAI/E-cadherin. [score:1]
C. Quantitative results are illustrated for panel B. NC: negative control; miR-625-3p: miR-625-3p mimic. [score:1]
SW480 cells were transfected with miR-625-3p mimics (Invitrogen, Shanghai, China) or a miR-625-3p mimics control (negative control, NC) (Invitrogen) using the Lipofectamine 2000 reagent (Invitrogen) following the manufacturer’s protocol. [score:1]
We also determine whether E-cadherin/MMP-9 pathway is involved in miR-625-3p -mediated tumorigenesis in CRC. [score:1]
However, the mechanism and function of miR-625-3p in CRC have not been fully determined. [score:1]
Figure 4NC: negative control; miR-625-3p: miR-625-3p mimic. [score:1]
Therefore, we also investigated the expression of MMP-9 in miR-625-3p -transfected SW480 cells. [score:1]
Interestingly, miR-625-3p was not associated with recurrence of stage II or III disease [29], indicating that further investigation is required to determine the role of miR-625-3p in CRC. [score:1]
miR-625–3p transfection. [score:1]
Figure 1NC: negative control; miR-625-3p: miR-625-3p mimic. [score:1]
To better understand the association between miR-625-3p and cell invasion, the baseline expression of miR-625-3p was measured in a panel of human colorectal cancer cell lines that included SW480, SW620, HT29, HCT116, and Colo205. [score:1]
Our results indicated that miR-625-3p could promote cell invasion in CRC cells. [score:1]
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miR-625 inhibits cell proliferation and clonogenicity of malignant melanoma cells in vitroBecause miR-625 is significantly downregulated in malignant melanoma, it might function as a tumor suppressor. [score:8]
This result strongly indicates that 3′UTR of SOX2 carries the direct binding seed of miR-625, and miR-625 might target SOX2 and inhibit its expression. [score:8]
The down-regulation of miR-625 removes the suppression of its target, SOX2, leading to promotion of the tumorigenicity in malignant melanoma. [score:8]
Our study shows that the expression level of miR-625 is inversely correlated with the expression profile of SOX2, and SOX2 reversed the inhibitory effect of miR-625 in malignant melanoma. [score:7]
Through analysis of the related microRNA array data, we found that the abnormal expression of miR-625 is associated with malignancy or the development process in many types of tumors (Figure 1A) [14, 16, 18, 19]], and it was one of downregulated microRNAs in the highly invasive melanoma cell lines [17]. [score:7]
The results showed that ectopic expression of miR-625 significantly suppressed migration and invasion of malignant melanoma cells, whereas knockdown of miR-625 by anti-sense oligos significantly enhanced migration and invasion. [score:6]
Because miR-625 is significantly downregulated in malignant melanoma, it might function as a tumor suppressor. [score:6]
In these studies, the expression levels of miR-625 were significantly lower in tumor tissue or cells compared with corresponding normal tissue or cells, and miR-625 inhibits proliferation, invasion and tumorigenesis in vitro or in vivo, suggesting that it may serve as a tumor suppressor. [score:6]
The function of tumor suppressor miR-625 is at least partially related to targeting and repressing SOX2, (Figure 8). [score:5]
miR-625 targets the 3′-UTR of SOX2To identify how miR-625 functions in malignant melanoma cells, computational prediction of miR-625 targets was performed. [score:5]
miR-625 suppresses the tumorgenicity and progression of malignant melanoma, suggesting that miR-625 will become a novel diagnostic marker and a new therapeutic target of malignant melanoma. [score:5]
Results suggested that reduction of miR-625 occurs in approximately 75% of human malignant melanoma (27/36 samples, Figure 1B), and the average relative expression level of miR-625 is significantly downregulated in tumor tissue compared with the non-tumor tissue (Figure 1C, * P < 0.05). [score:5]
miR-625 suppresses tumorigenicity of malignant melanoma cells in nude mice in vivoWe next validated whether ectopic expression of miR-625 influences the tumor growth of malignant melanoma cells in vivo. [score:5]
Ectopic expression of miR-625 mimics suggested that miR-625 suppresses proliferation, wound healing, migration and invasion in malignant melanoma cells. [score:5]
As shown in the Figure 5A-5C, the tumors grew progressively in the control group, but were suppressed in the miR-625 ectopic expression group. [score:5]
miR-625 mimics, negative control mimics, miR-625 inhibitors (anti-miR-625) and inhibitor controls (anti-miR-NC) were purchased from GenePharma (Shanghai, Ch ina). [score:5]
The result showed that the average relative expression level of miR-625 was significantly upregulated in tumor tissue compared with non-tumor tissue (Figure 6C). [score:5]
The results showed that ectopic expression of SOX2 reversed the inhibitory effect of miR-625 on cell proliferation (Figure 7A and 7B) and migration (Figure 7C-7F) in malignant melanoma. [score:5]
These studies show that miR-625 is frequently deregulated in tumor tissue or cells, and the decreased expression of miR-625 correlated with the invasiveness and metastasis predict high malignancy and poor prognosis. [score:4]
Our data show that miR-625 is frequently downregulated in malignant melanoma. [score:4]
miR-625 is downregulated in malignant melanoma tissues. [score:4]
F. miR-625 mimics downregulated luciferase activities controlled by wild-type SOX2 3′UTR, but did not affect luciferase activity controlled by mutant SOX2 3′UTR. [score:4]
A recent study indicates that miR-625 is one of the miRNAs that are downregulated in highly invasive malignant melanoma cells [17]. [score:4]
miR-625 is downregulated in human malignant melanoma. [score:4]
miR-625 inhibits migration and invasion of malignant melanoma cells. [score:3]
We found that SOX2 is a potential target of miR-625 in malignant melanoma. [score:3]
Since SOX2 is a potential target of miR-625, it is reasoned that ectopic of SOX2 could rescue the biological phenotypes caused by miR-625 in malignant melanoma. [score:3]
miR-625 inhibits wound-healing ability of malignant melanoma cells. [score:3]
Moreover, SOX2 expression levels were inversely correlated with miR-625 levels in tissues (Figure 6D). [score:3]
Thus, these results indicate that miR-625 suppresses tumorigenesis of malignant melanoma cells in vivo. [score:3]
D. Linear correlation analysis of SOX2 and miR-625 expression in melanoma samples. [score:3]
Figure 6miR-625 targets the 3′-UTR of SOX2 A-B. The putative binding sites of miR-625 in the SOX2 3′-UTR region were predicted by miRanda. [score:3]
Thus, the data provide evidence that inhibition by miR-625 is at least partially related to the function of SOX2. [score:3]
SOX2 can rescue effect of miR-625 in malignant melanoma cellsSince SOX2 is a potential target of miR-625, it is reasoned that ectopic of SOX2 could rescue the biological phenotypes caused by miR-625 in malignant melanoma. [score:3]
miR-625 inhibits cell proliferation and clonogenicity of malignant melanoma cells in vitro. [score:3]
To examine the expression levels of miR-625 in malignant melanoma tissue and normal tissue, we performed qRT-PCR analysis on 36 malignant melanoma samples. [score:3]
miR-625 inhibits tumorigenicity of malignant melanoma cells in vivo. [score:3]
miR-625 suppresses migration and invasion of malignant melanoma cells in vitro. [score:3]
To identify how miR-625 functions in malignant melanoma cells, computational prediction of miR-625 targets was performed. [score:3]
The nude mouse subcutaneous tumor formation mo del confirmed that miR-625 inhibits the tumorgenicity in malignant melanoma cells in vivo, which is an important aspect of tumor progression. [score:3]
These findings indicate that miR-625 inhibits proliferation and colony-forming ability of malignant melanoma cells. [score:3]
miR-625 suppresses tumorigenicity of malignant melanoma cells in nude mice in vivo. [score:3]
miR-625 inhibits proliferation, migration, and invasion in melanoma. [score:3]
miR-625 inhibits scratch wound-healing ability of malignant melanoma cells. [score:3]
It has been reported that miR-625 targets HMGA1, SCAI, IGF2BP1, and ILK [12– 16]. [score:3]
Figure 5miR-625 inhibits tumorigenicity of malignant melanoma cells in vivo A-C. Photographs of tumors derived for pSilencer-miR-Control or pSilencer-miR-625 stably transfected A375 cells in nude mice. [score:3]
We next validated whether ectopic expression of miR-625 influences the tumor growth of malignant melanoma cells in vivo. [score:3]
miR-625 suppresses migration and invasion of malignant melanoma cells in vitroTo further assess the influence of miR-625 on malignant melanoma cells, we explored its effects on cell migration and invasion, a key factor in tumor progression and metastasis. [score:3]
miR-625 targets the 3′-UTR of SOX2. [score:3]
The genes predicted by all the programs were considered candidate targets of miR-625. [score:2]
Therefore, we determined whether deregulation of miR-625 in malignant melanoma cells correlates with cell proliferation. [score:2]
miR-625 deregulation has been detected in many cancers, including breast cancer [12], colorectal carcinoma [13], hepatocellular carcinoma [14], squamous cell carcinoma [15], and gastric cancer [16]. [score:2]
As a negative regulator of SOX2, miR-625 has potential value in precision medical therapy. [score:2]
In the present study, we found that the expression of miR-625 decreased significantly in malignant melanoma tissue compared with the normal tissue. [score:2]
Restoration of the miR-625 overexpressing cell line A375 [miR-625] slowly closed the scratch wounds compared with the control group 36 hours after scratching. [score:2]
Deregulation of miR-625 has been reported in various cancers [12– 16]. [score:2]
The relative luciferase activity of the SOX2-3′UTR [wt] reporter was apparently suppressed by miR-625 mimics compared with that of SOX2-3′UTR [mut] in an miR-625 -dependent manner (Figure 6F). [score:2]
E. Schematic graph of the putative binding sites of miR-625 in the SOX2 3′UTR and the mutation in miR-625 binding sites. [score:2]
C. Relative expression of miR-625 in malignant melanoma patients’ tumor tissues compared with normal tissues. [score:2]
B. M14 cells were transfected with miR-625 mimics, NC mimics, anti-625, or anti-NC at a final concentration of 100 nM, at 24 hours after transfection. [score:1]
E. Representative photographs of migratory M14 [NC mimics+Vector], M14 [miR-625+Vector], and M14 [miR-625+SOX2] cells on the membrane (magnification, 100×). [score:1]
These findings suggest that miR-625/ SOX2 is an important factor in malignant melanoma tumorigenesis. [score:1]
C. Representative photographs of migratory or invasive M14 [NC mimics], M14 [miR-625], M14 [anti-NC], or M14 [anti-miR-625] cells on the membrane (magnification, 100×). [score:1]
Results are means of three independent experiments ± S. D. C. Representative photographs of migratory A375 [NC mimics+Vector], A375 [miR-625+Vector], and A375 [miR-625+SOX2] cells on the membrane (magnification, 100×). [score:1]
Figure 4 A. Representative photographs of migratory or invasive A375 [NC mimics], A375 [miR-625], A375 [anti-NC], or A375 [anti-miR-625] cells on the membrane (magnification, 100×). [score:1]
B. miR-625 was detected in melanoma tissues. [score:1]
To explore the contribution of miR-625 in vivo, we carried out mouse xenograft mo dels. [score:1]
As shown in Figure 4, the number of migratory and invasive A375 cells transfected with miR-625 mimics was significantly less than the control group, whereas the number of A375 cells transfected with anti-miR-625 was higher than the control group (** P < 0.01, Figure 4A and 4B), and the results of the M14 cell groups are also consistent. [score:1]
In contrast, the A375 [anti-miR-625] cells were significantly efficient in wound healing (Figure 3B). [score:1]
Strikingly, the tumor volumes and weights in the A375 [miR-625] group were significantly less than the volumes and weights in the control group. [score:1]
A375 cells were transfected with miR-625 mimics, NC mimics, anti-625, or anti-NC, and then seeded onto 6-well plates. [score:1]
miR-625 is an overlapping candidate. [score:1]
A. Representative photographs of migratory or invasive A375 [NC mimics], A375 [miR-625], A375 [anti-NC], or A375 [anti-miR-625] cells on the membrane (magnification, 100×). [score:1]
Moreover, SOX2 rescued the effect of miR-625 on sphere formation, which is necessary for cell self-renewal (Figure 7E-7I). [score:1]
D. Average number of migratory or invasive M14 [NC mimics], M14 [miR-625], M14 [anti-NC], or M14 [anti-miR-625] cells (* P < 0.05, ** P < 0.01). [score:1]
Schematic graph depicting the function of miR-625 in malignant melanoma. [score:1]
However, the function of miR-625 in malignant melanoma is largely unknown. [score:1]
Malignant melanoma cells A375 transfected with miR-625 mimics or control mimics were selected and injected subcutaneously into nude mice, and the tumor formation was monitored. [score:1]
A-B. The putative binding sites of miR-625 in the SOX2 3′-UTR region were predicted by miRanda. [score:1]
B. Average number of migratory or invasive A375 [NC mimics], A375 [miR-625], A375 [anti-NC], or A375 [anti-miR-625] cells. [score:1]
SOX2 can rescue effect of miR-625 in malignant melanoma cells. [score:1]
The number of colonies from A375 [miR-625] and M14 [miR-625] cells were fewer than the number of colonies from control groups A375 [NC mimics] and M14 [NC mimics], and the number of colonies from A375 [anti-miR-625] and M14 [anti-miR-625] cells were higher than the number of colonies from control groups A375 [NC mimics] and M14 [NC mimics] (* P < 0.05, ** P < 0.01, Figure 2E and 2F). [score:1]
To further assess the influence of miR-625 on malignant melanoma cells, we explored its effects on cell migration and invasion, a key factor in tumor progression and metastasis. [score:1]
Our data show that miR-625 is an important factor in the migration and invasion ability of malignant melanoma cells. [score:1]
The results showed that cell growth was inhibited in the group transfected with miR-625 mimics compared with the cells transfected with control mimics, and the cell growth was promoted by anti-miR-625 compared with the anti -negative control (NC) oligos. [score:1]
The effect of miR-625 on the proliferation of malignant melanoma cells. [score:1]
Results are means of three independent experiments ± S. D. B. M14 cells were transfected with miR-625 mimics, NC mimics, anti-625, or anti-NC at a final concentration of 100 nM and, at 24 hours after transfection. [score:1]
SOX2 can rescue effect of miR-625 in malignant melanoma. [score:1]
A375 cells were transfected with miR-625 mimics, NC mimics, anti-625, or anti-NC at a final concentration of 100 nM, at 24 hours after transfection. [score:1]
A375 cells were transfected with miR-625 mimics, NC mimics, SOX2, or Vector control, at 24 hours after transfection. [score:1]
A-C. Photographs of tumors derived for pSilencer-miR-Control or pSilencer-miR-625 stably transfected A375 cells in nude mice. [score:1]
Then we performed luciferase reporter assays to verify a direct interaction between miR-625 and the 3′UTR of SOX2. [score:1]
D. M14 cells were transfected with miR-625 mimics, NC mimics, anti-625, or anti-NC, and then seeded onto 6-well plates. [score:1]
Luciferase reporters were constructed with either a wild-type SOX2 3′UTR sequence that contained the miR-625 binding site (SOX2-3′UTR [wt]) or a mutated 3′UTR (SOX2-3′UTR [mut]) (Figure 6E). [score:1]
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5
[+] score: 77
The significance of the differences in the expression was confirmed for four of the miRNAs, including three down-regulated miRNAs namely miR-181d-5p, miR-140-3p and miR-206 and one up-regulated miRNA namely miR-625-5p) (P < 0.05) (Fig.   2). [score:9]
The significance of the differences in the expression was confirmed for four of the miRNAs, including three down-regulated miRNAs namely miR-181d-5p, miR-140-3p and miR-206 and one up-regulated miRNA namely miR-625-5p (P < 0.05) (Fig.   1). [score:9]
The significance of the differences in the expression was confirmed for six of the miRNAs, including two down-regulated miRNAs namely miR-181d-5p and miR-206 and four up-regulated miRNA namely miR-1233-3p, miR-183-5p, miR-421 and miR-625-5p) (P < 0.05) (Fig.   3). [score:9]
In detail, we selected two miRNAs with high fold changes among the up-regulated (miR-625-5p and miR-183-5p) and four miRNAs with high fold changes among the down-regulated ones (miR-181d-5p, miR-206, miR-142-5p and miR-339-5p). [score:7]
To gain insights into the potential impact of the three validated miRNAs (miR-181d-5p, miR-206 and miR-625-5p) in regulating target genes, we applied miRTargetLink [23]. [score:6]
Moreover, differential expression levels of miR-421, miR-1233-3p and miR-625-5p were found in TOF-noHF and TOF-HF patients with significantly reduced expression levels in TOF patients with symptomatic right heart failure (Fig.   4). [score:5]
Expression levels of miR-421, miR-1233-3p and miR-625-5p are lower in TOF patients with symptomatic right heart failure and thus may indicate disease progression in these patients. [score:5]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for six miRNAs namely miR-181d-5p, miR-1233-3p, miR-183-5p, miR-206, miR-421 and miR-625-5p. [score:4]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for five miRNAs namely miR-181d-5p, miR-142-5p, miR-206, miR-339-5p and miR-625-5p. [score:4]
We found that expression levels of circulating miR-421, miR-1233-3p and miR-625-5p were significantly lower in TOF patients with as compared to those without symptomatic right heart failure indicating a potential role of these miRNAs in identifying disease progression in TOF patients. [score:4]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for six miRNAs namely miR-181d-5p, miR-142-5p, miR-1233-3p, miR-206, miR-339-5p and miR-625-5p. [score:4]
Bioinformatics analysis helped to gain insights into the potential impact of the three validated miRNAs (miR-181d-5p, miR-206 and miR-625-5p) on target genes (Additional file 3: Figure S2). [score:3]
Moreover, expression levels of miR-625-5p, miR-1233-3p and miR-421 were lower in TOF-HF compared to TOF-noHF (P = 0.012). [score:2]
Together, the three miRNAs namely miR-181d-5p, miR-206 and miR-625-5p were significantly deregulated in all subgroups of TOF patients. [score:2]
The diagnostic accuracy of only three of the validated miRNAs namely miR-181d-5p, miR-206 and miR-625-5p by ROC analysis was high with AUCs of 0.987, 0.993 and 0.769 respectively in all TOF patients and 0.990, 0.994 and 0.749 respectively in the subset of TOF patients without symptomatic right heart failure. [score:1]
Three miRNAs namely miR-181d-5p, miR-206 and miR-625-5p were validated by RT-qPCR in all TOF groups. [score:1]
It is of note, however, that miR-625-5p showed the highest fold change between healthy controls and the subset of TOF patients with symptomatic right heart failure. [score:1]
These results indicate the high diagnostic accuracy of miR-181d-5p and miR-206 and a moderate accuracy of miR-625-5p in differentiating TOF patients from healthy controls. [score:1]
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6
[+] score: 30
We found that miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 were highly upregulated just in cells with HPV infection upon 5-AZA treatment, whereas miR-625 was significantly downregulated (P<0.05) (Figure  3). [score:7]
ILK is a direct target gene for miR-625 and knockdown of ILK has a phenocopy of overexpression of miR-625 (Wang M, et al., [25]). [score:7]
Expression of miR-625 is significantly down-regulated and negatively correlated with lymph node metastasis in gastric cancer. [score:6]
Increasing evidence points to a central role of miR-625 for vesicle trafficking processes in oncogenesis and tumor suppression. [score:3]
In the hormonal treatment of endometrial carcinoma, Hec1A cells were treated with medroxyprogesterone acetate, the expression levels of miR-625 was increased by more than 400% (Bae J, et al., [26]). [score:3]
MiR-625 significantly inhibits invasion and metastasis of gastric cancer cells both in vitro and in vivo. [score:2]
MiR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 were found up-modulated in Caski, Hela and Siha but not in C33A induced on treatment, while miR-625 was down-modulated. [score:1]
In our study, we found miR-625 was decreased after demethylation. [score:1]
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7
[+] score: 28
a High level of six hsa-miRNAs randomly selected for the validation of expression level by qRT-PCR is consistent with the result from miRNA microarray; b Low level of six hsa-miRNAs randomly selected for the validation of expression level by real-time RT-PCR is consistent with the result from miRNA microarray Fig.  3Validation of 12 hsa-miRNAs using qRT PCR shows hsa-mir-1267, hsa-miR-4309, hsa-miR-554, hsa-miR-1272, hsa-miR-4501, hsa-miR-182-3p were up-regulated and hsa-miR-625-5p, hsa-miR-100-5p, hsa-miR-125b-5p, hsa-miR-197-3p, hsa-miR-4522, hsa-miR-493-5p were down-regulated in each of the peripheral blood samples from narcolepsy patients. [score:11]
Consistent with the results from the microRNA microarray (Fig.   2a, b), hsa-mir-1267, hsa-miR-4309, hsa-miR-554, hsa-miR-1272, hsa-miR-4501, hsa-miR-182-3p were up-regulated and hsa-miR-625-5p, hsa-miR-100-5p, hsa-miR-125b-5p, hsa-miR-197-3p, hsa-miR-4522, hsa-miR-493-5p were down-regulated in each of the peripheral blood samples (Fig.   3). [score:7]
Among these miRNAs with significant change, 12 hsa-miRNAs were validated by qRT PCR which showed that hsa-mir-1267, hsa-miR-4309, hsa-miR-554, hsa-miR-1272, hsa-miR-4501, hsa-miR-182-3p had significantly high expression and hsa-miR-625-5p, hsa-miR-100-5p, hsa-miR-125b-5p, hsa-miR-197-3p, hsa-miR-4522, hsa-miR-493-5p had significantly low expression in each of the peripheral blood samples. [score:5]
For example, miR-625-5p may act as one of potential mediators of hypoxic response in soft tissue sarcomas (STS); miR-100-5p appeared to be important to regulation some gene expression during GC reaction. [score:4]
In conclusion, we have identified 12 aberrant miRNAs (hsa-mir-1267, hsa-miR-4309, hsa-miR-554, hsa-miR-1272, hsa-miR-4501, hsa-miR-182-3p, hsa-miR-625-5p, hsa-miR-100-5p, hsa-miR-125b-5p, hsa-miR-197-3p, hsa-miR-4522, hsa-miR-493-5p) in plasma from patients with sleep disorder. [score:1]
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8
[+] score: 13
Tested miRNAs (Table 1) included the 32 mentioned above; 6 additional miRNAs that appeared in more recent versions of the miRbase database and had putative target sites in the truncated isoform (miR-485-3p, miR-509, miR-617, miR-625, miR-765 and miR-768-5p) were also included because allelic variants were found in their target sites after re-sequencing of patients with anxiety disorders [19]. [score:5]
The remaining four miRNAs (miR-324-5p, miR-330-3p, miR-509 and miR-625) caused a slight reduction in the expression levels of the truncated isoform of NTRK3 (maximum 15%), but none of them reached statistical significance. [score:3]
The most conspicuous inhibition was detected with miR-625 (62% reduction), miR-509 (47%) and miR-128 (32%), while the other five miRNAs gave a reduction ranging between 13% and 30%. [score:3]
Luciferase-validated miRNAs were therefore transfected into either undifferentiated (miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p) or differentiated SH-SY5Y cells (miR-151-3p and miR-185), and protein levels were assessed by western blotting 72 h after transfection. [score:1]
In the case of pGL4.13-TR, the luciferase activity was significantly reduced by 8 miRNAs (Figure 1A), all of which were predicted by at least one program: miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p. [score:1]
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9
[+] score: 12
To explore the mechanisms underlying the upregulation of miRNAs in endometrial cancers, we examined the methylation status of miR-130a, miR-130b, miR-625 and miR-200b by bisulfite-specific PCR sequencing (Table  1). [score:4]
In this present study we found that aberrant expression of miRNAs including miR-200b, miR130a/b, miR-625 and miR-222 was associated with tumorigenesis and metastasis in endometrial cancer. [score:3]
Aberrant expression of miRNAs including miR-200b, miR-130a/b, miR-625 and miR-222 was associated with tumorigenesis and metastasis in endometrial cancer. [score:3]
miR-130a/b, miR-200b, and miR-625 contain several CpG sites in their upstream regulatory sequences. [score:2]
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10
[+] score: 11
Statistically significant downregulation of miR-126 (p < 0.001) between mesothelioma cases and asbestos-exposed controls could be observed in contrast to miR-625-3p (Additional File 5). [score:4]
For mesothelioma, a multitude of deregulated miRNAs in tissues and cell lines was described [10– 18], whereas only three blood -based miRNAs, namely, miR-103a-3p [19], miR-126 [20], and miR-625-3p [21], were identified as potential biomarkers. [score:2]
Thus, for combination analysis, miR-126 was selected, whereas miR-625-3p was excluded from further analysis. [score:1]
Whereas miR-625-3p failed to show a significant difference in this study, miR-126 discriminated between cancer cases and controls. [score:1]
The two miRNAs miR-126 (U6 snRNA as reference) and miR-625-3p (miR-16 as reference) were previously described as circulating biomarkers for mesothelioma [20, 21]. [score:1]
Notably, miR-126 and miR-625-3p are not affected by hemolysis [55]. [score:1]
Thus, two already described circulating miRNAs, namely, miR-126 [20] and miR-625-3p [21], were additionally analyzed in this study group. [score:1]
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11
[+] score: 10
However, we identified 8 miRNAs exclusively expressed in FSHD1 samples (miR-330, miR-331-5p, miR-34a, miR-380-3p, miR-516b, miR-582-5p, miR-517* and miR-625) which could represent new biomarkers for this disease. [score:5]
For example, miR-516b, miR-582–5p and miR-625 target AKAP2, which was identified in skeletal muscle, brain and testis, to be involved in the cAMP signaling pathway [59]. [score:3]
We did not observed any miRNAs only detected in control samples but we identified 8 miRNAs which were only expressed in FSHD samples as compared to age-matched controls: miR-330, miR-331–5p, miR-34a, miR-380–3p, miR-516b, miR-582–5p, miR-517* and miR-625. [score:2]
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12
[+] score: 7
The expression profile of infected and uninfected cells was evaluated using a miRNA microarray, and 16 miRNAs were reported to be up-regulated (miR-4290, miR-4279, miR-625*, miR-let-7e, miR-1290, miR-33a, miR-3686, miR-378, miR-1246, miR-767-5p, miR-320c, miR-720, miR-491-3p, miR-3647, miR-451 and miR-4286) and 4 down-regulated (miR-106b, miR-20a, miR-30b and miR-3653) during dengue infection. [score:7]
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13
[+] score: 6
Compared to ALK(−) ALCLs, miR-203, miR-135b, miR-886-5p/3p, miR-20b, miR-106a and miR-183 were significantly upregulated in ALK(+) ALCLs while others (miR-155, miR-181a, miR-210, miR-29a/b, miR-342-5p/3p, miR-369-3p miR-374a/b, miR-423-5p, miR-625, miR-205, miR-146a and miR-26a) were down-regulated (Table 1). [score:6]
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14
[+] score: 6
Furthermore, miRNAs have a role in the course of therapy; patients with lung cancer who have undergone surgical treatment show an increase in miR-625 and miR-361-3p, with similar expression levels as those in individuals with benign diseases and healthy persons, emphasizing that these miRNAs might have a protective influence on the development of lung cancer [54]. [score:6]
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15
[+] score: 6
In addition, miR-625 expression is significantly downregulated and inversely associated with lymph node metastasis of gastric cancer [14]. [score:6]
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16
[+] score: 5
Alterations in miRNA expression have been observed in CRC, and several dysregulated miRNAs, including miR-625-3p [8], miR-99-5b [9], miR-361-5p [10], miR-17-5p [11], miR-137 [12], miR-95 [13], miR-23a [14, 15], miR-155 [16], miR-150 [17], miR-191[18], miR-339-5p [19], miR-429 [20], miR-345 [21], miR-22 [22], miR-638 [23] and miR-138 [24], have been shown to regulate CRC cell growth, apoptosis and metastasis. [score:5]
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17
[+] score: 5
It was established that increased expression of miR-23a, miR-27a, miR-30c, let-7g, and miR-199a-3p corresponds to resistance to platinum -based chemotherapy while reduced expression of miR-378 and miR-625 relates to resistance. [score:5]
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18
[+] score: 5
A microarray analysis found six miRNAs (miR-148a, miR-181a, miR-20a, miR-221, miR-625 and miR-99b) that were upregulated in patients with MM compared to healthy controls [20]; miR-221 and miR-99b were related to the karyotype of the disease, whereas miR-148a and miR20a were related to relapse-free survival [20]. [score:5]
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19
[+] score: 5
miR-625 suppresses hepatocellular carcinoma migration and invasion by targeting IGF2BP1 and further affects the IGF2BP1/PTEN pathway [36]. [score:5]
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20
[+] score: 5
For example, miR-625, miR-103/miR-107, miR-21 and miR-301 have been found to promote CRC to invade and metastasize by stimulating multiple metastasis-promoting genes [27– 30], whereas miR-99, miR-137, miR-132 and miR-128 function as tumor suppressors to inhibit the metastasis of CRC [31– 34]. [score:5]
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21
[+] score: 4
Down-regulation of Dicer was followed by decreased production of several miRNAs (miR1301, miR1249, miR1227, miR532-3p, miR625, miR1827, miR324-5p) as assessed by real-time PCR (data not shown). [score:4]
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[+] score: 4
In contrast, 11 miRNAs (miR-9-5p, miR-184, miR-328-3p, miR-363-3p, miR-372-3p, miR-518d-3p, miR-518f-3p miR-523-3p, miR-618, miR-625-5p, and miR-628-5p) were significantly up-regulated in human oocytes (with respect to FF) (Figure 3B and Supplementary Table S1). [score:4]
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23
[+] score: 4
However, miR-215 [31], miR-375 [32], miR-141, and miR-200c [33], miR-200a [34], miR-429 [35], miR-625 [36], and miR-18a [37] have already been shown to be inversely correlated with the EMT, and they were found downregulated in this subtype. [score:4]
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24
[+] score: 4
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Indeed, although CTNNA2 can be regulated by primate-specific miRNAs common to both monkeys and humans (miR-513a-3p, miR-518a-5p, miR-548a-5p, miR-576-5p, miR-586, miR-607, miR-625, miR-642), a number of miRNAs present in Homo sapiens but not in Macaca mulatta (miR-1208, miR-1247, miR-1290, miR-1324, miR-1825, miR-613 and miR-634) also target CTNNA2 [19], [29]. [score:4]
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25
[+] score: 4
miR-625 showed increased expression in dMMR tumors and unchanged in pMMR tumors, relative to normal tumors. [score:3]
In contrast, miR-625 and miR-31 exhibited increased levels in dMMR relative to pMMR tumors. [score:1]
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26
[+] 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]
No significant difference was found for glomerular miR-133a-3p, miR-138-5p, miR-146b-5p or miR-625-3p. [score:1]
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27
[+] score: 3
Other miRNAs from this paper: hsa-mir-28, hsa-mir-409
Among these differentially expressed miRNAs, several have been reported in previous studies, such as miRlet-7, miR409, miR-28-5p, miR-625, etc. [score:3]
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[+] score: 3
Additional miRNAs involved in the regulation of the AhR include has-mir-26a-5p, hsa-mir-130b-3p, has-mir-124-3p, has-miR-625-5p and has-miR-98-5p with proven experimental evidence for their participation in the regulation of genes coding for lipid transport most notable CD36, fatty acid binding proteins FABP1, FAB6, FAB7, low density lipoprotein receptor, RXRß and others based on miRTarBase data analysis and PubMed searches. [score:3]
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29
[+] 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-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-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
Differential expression of miR-18a, miR-532, miR-218, miR-625, miR-193a, miR-638, miR-550 and miR-633 can be used as a marker to predict prednisone response in pediatric ALL patients [76]. [score:3]
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[+] 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-505, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, 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 the current study, we identified three typical miRNA* species (miR-149*, miR-625* and miR-9*) that were exclusively expressed in the L1- silenced cells with normalized read counts ≥ 10 (Supplementary Table S1). [score:3]
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[+] score: 2
ANKS6 9q22.33 F HUB unknownmiR-125a-5p miR-125b-5p ARHGAP1 11p11.2 F HUB T-cell development C11orf24 11q13 F HUB Golgi/ERmiR-193b-3p [b] LAPTM4B 8q22.1 F HHUB Autophagy miR-625-5p CYFIP1 15q11 H VIP Golgi/ER miR497-5p a Comm: Community b validated miRNA-gene interaction (miRTarBase databank); ER: endoplasmic reticulum. [score:2]
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[+] score: 1
79 ** hsa-mir-365 7.13 *** 77.53 *** hsa-mir-429 54.63 *** 85.25 *** hsa-mir-454 33.25 *** 87.31 - hsa-mir-455-3p 42.76 *** 96.4 - hsa-mir-484 4.83 *** 78.73 - hsa-mir-485-3p 4.75 *** 71.49 *** hsa-mir-501-3p 69.25 *** 91.25 *** hsa-mir-512-5p 21.37 *** 72.89 *** hsa-mir-532-3p 9.5 *** 85.93 *** hsa-mir-541 69.87 *** 97.77 - hsa-mir-600 35.63 *** 93.48 - hsa-mir-625* 28.5 *** 72.89 *** 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-636 2.37 *** 81.98 *** hsa-mir-663 21.38 *** 84.73 *** hsa-mir-664 7.13 *** 82.85 *** hsa-mir-766 45.13 *** 73. [score:1]
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[+] score: 1
For the pre-miRNAs originally annotated to encode miRNAs at both arms, the major arms of hsa-mir-374a, hsa-mir-500a, hsa-mir-625 and hsa-mir-136 are their 5p arms; while, the major arms of hsa-mir-664, hsa-mir-144, hsa-mir-493 and hsa-mir-376a-1 are their 3p arms. [score:1]
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[+] score: 1
Surprisingly, out of these, only two miRNAs (miR-23a-5p, miR-137) were more abundant in sEVs at both time points (Fig. 5C), while five miRNAs (miR-17-3p, miR-625-3p, miR-766-3p, miR-199b-5p, miR-381-3p) were less abundant in sEVs of senescent cells (Fig. 5D). [score:1]
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[+] score: 1
The following are the 10 miRNA precursors with previously unreported antisense transcripts: hsa-miR-33b, hsa-miR-101, hsa-miR-191, hsa-miR-219-2, hsa-miR-374b, hsa-miR-486, hsa-miR-625, hsa-miR-766, hsa-miR-3135b, and hsa-miR-4433. [score:1]
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[+] score: 1
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-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-218-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-128-1, hsa-mir-145, hsa-mir-191, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-361, hsa-mir-337, hsa-mir-148b, hsa-mir-196b, hsa-mir-425, hsa-mir-20b, hsa-mir-486-1, hsa-mir-488, hsa-mir-181d, hsa-mir-498, hsa-mir-519c, hsa-mir-520a, hsa-mir-526b, hsa-mir-520d, hsa-mir-506, hsa-mir-92b, hsa-mir-608, hsa-mir-617, hsa-mir-641, hsa-mir-1264, hsa-mir-1271, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-128-1, bta-mir-145, bta-mir-181a-2, bta-mir-30b, bta-mir-181b-2, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-148b, bta-mir-181c, bta-mir-191, bta-mir-210, bta-mir-23a, bta-mir-361, bta-mir-425, bta-let-7g, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-99b, hsa-mir-890, hsa-mir-888, hsa-mir-889, hsa-mir-938, hsa-mir-1184-1, hsa-mir-1203, hsa-mir-1204, hsa-mir-1265, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-218-1, bta-mir-296, bta-mir-30f, bta-mir-486, bta-mir-488, bta-mir-92a-1, bta-mir-92b, bta-mir-1271, bta-mir-181a-1, bta-mir-181b-1, bta-mir-148c, hsa-mir-1184-2, hsa-mir-1184-3, hsa-mir-486-2, bta-mir-1264, bta-mir-148d
Among these, miR-938, miR-519c-3p, miR-1265, miR-498 and miR-488 were exclusively detected only in HE animals and 10 miRNAs including miR-608, miR-625*, miR-218-1*, miR-888*, miR-1184 and miR-1264 were detected only in SE and CE animal groups. [score:1]
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[+] score: 1
Comparing the AS to control groups, we confirmed differences in levels of miR-122-5p (Mann-Whitney p < 0.0001), miR-21-5p (p < 0.0001), miR-625-5p (p = 0.017), miR-221-3p (p < 0.0001) and miR-30e-5p (p = 0.012). [score:1]
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[+] score: 1
MiRNAs miR-135b-3p, miR-146b-5p, miR-205-5p, miR-425-3p, miR-625-3p, and miR-485-3p which are involved in signaling and cell migration connected with epithelial to mesenchymal transition, tumor invasion, and metastasis, were detected in both the comparison of HPV immortalized keratinocytes with primary keratinocytes and the comparison of telomerase immortalized clones with primary keratinocytes. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
The miRNAs that are most affected are miR-185, miR-625, miR-203, and miR-429. [score:1]
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However, six miRNAs (miR-17, miR-202, miR-425, miR-493, miR-624 and miR-625) had a higher number of sequencing reads originating from the annotated miRNA* strand than the mature miRNA sequence across majority of the libraries (Additional File 3). [score:1]
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