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49 publications mentioning hsa-mir-190b

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-190b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 297
Overexpression of miR-190b in Huh7 cells attenuated the expression of IGF-1, whereas inhibition of miR-190b resulted in up-regulation of IGF-1. Restoration of IGF-1 expression reversed miR-190b -mediated impaired insulin signaling in Huh7 cells, supporting that IGF-1 was a direct and functional target of miR-190b. [score:15]
Because inhibition of expression by miRNA may also be mediated by mRNA degradation, we examined whether IGF-1 mRNA levels might be affected by miR-190b; consistent overexpression of miR-190b decreased IGF-1 mRNA levels, whereas inhibition of miR-190b increased the levels (Figure 3D), indicating that miR-190b might act to destabilize or degrade IGF-1 mRNA transcripts. [score:9]
Over -expression of miR-190b Contributes to Hepatic Insulin Resistance through Down-regulation of IGF-1 Expression. [score:8]
Over -expression of miR-190b in HCC cells leads to insulin resistance through down-regulation of IGF-1 expression. [score:8]
Conversely, increased expression of IGF-1 was observed in stable cells expressing miR-190b inhibitor (Figure 3B, right). [score:7]
Specific miRNA (miR)-190b, which was significantly up-regulated in HCC tumor tissues when compared with paired non-tumor tissues, was among those predicted to interact with 3′-untranslated region (UTR) of IGF-1. In order to explore the regulatory effects of miR-190b on IGF-1 expression, luciferase reporter assay, quantitative real-time PCR, western blotting and immunofluorecence analysis were performed in HCC cells. [score:7]
The EGFP-tagged pEZX-MR04 vectors expressing precursor miR-190b and scrambled sequences [named pre-miR-190b and pre -negative control (NC)], the mCherry-tagged pEZX-AM01 vectors expressing the miR-190b inhibitor and scrambled sequences (named anti-miR-190b and anti-NC), as well as luciferase vectors (pEZX-MT01) containing IGF-1 3′UTRs, were obtained from GeneCopoeia, Rockville MD. [score:7]
However, the principle of our inhibitor is to de-repress microRNA targets [22], so the transfected inhibitors would not alter the amount of endogenous miR-190b (Figure 3A, right). [score:7]
To learn whether miR-190b can affect endogenous IGF-1 protein levels, we established Huh7 stable cells that constitutively express precursor negative control, precursor miR-190b, inhibitor negative control or miR-190b inhibitor. [score:7]
of this study have shown that HCC significantly increases expression of miR-190b, which targets to IGF-1 3′UTR directly, resulting in impaired insulin signaling and gluconeogenesis. [score:6]
Collectively, these results indicate that IGF-1 gene expression is directly and post-transcriptionally suppressed by miR-190b. [score:6]
Next, we correlated the expression of IGF-1 to that of miR-190b in the 29 HCC tumor tissues and identified a marginally reverse correlation (P = 0.057; Figure 1D), implying that miR-190b dysregulation might be associated with the decline of IGF-1. Analysis of the 3′UTR sequence of IGF-1 using TargetScan revealed two possible binding sites for miR-190b at positions 844–850 and 1752–1758 (Figure 2A). [score:6]
The idea that tumor-specific factors also contribute to the decline of IGF-1 in HCC was supported by evidence that overexpressed miR-190b in HCC tumor tissues regulated IGF-1 expression. [score:6]
Conversely, IGF-1 expression in cells transfected with miR-190b inhibitor was increased when compared to inhibitor controls (Figure S2-A and B). [score:6]
Identification of miRNA that Targets IGF-1. IGF-1 is a Direct Target of miR-190b. [score:6]
As shown in Figure S3-D, increased expression of miR-190b inhibited cell apoptosis in HCC cells. [score:5]
As shown in Figure 2C, the suppressive effect of miR-190b was significantly reversed on mutation of binding site 2 (7mer-m8), whereas no significant changes were noted on mutation of binding site 1 (7mer-A1). [score:5]
Besides, we showed that the impaired insulin signaling caused by overexpression of miR-190b in HCC cells can partly reverse by restoring IGF-1 expression. [score:5]
The expression of miR-190b was significantly up-regulated in 66% (19/29) of HCC samples compared with the paired nontumor tissues (Figure 1C). [score:5]
Next, when exploring the corresponding IGF-1 protein levels in these stable clones, western blotting showed dose -dependent reduced expression of IGF-1 in Huh7 stable cells expressing precursor miR-190b (Figure 3B, left). [score:5]
We next asked whether the insulin-resistance effects of miR-190b in HCC cells was attributed to its suppressive effect on IGF-1 expression. [score:5]
Furthermore, inhibition of miR-190b in HepG2 cells led to a clear increase of IGF-1 expression both in the mRNA (Figure 3G) and protein levels (Figure 3H). [score:5]
Overexpression of miR-190b increased hepatic expression and insulin-stimulated phosphorylation of IRS1 (insulin receptor substrate-1) at Ser612 and Ser318 (Figure 5A), verifying impairment of insulin signaling [23]. [score:5]
Luciferase vectors and precursor control or precursor-miR-190b or inhibitor control or inhibitor miR-190b were co -transfected into cells using TurboFect reagent (Fermentas, Glen Burnie, MD, USA) following the manufacturer’s protocol. [score:5]
analysis was used to further confirm the relationship between miR-190b and IGF-1. Representative staining is shown in Figure S2-C and D. IGF-1 expression was suppressed in cells transfected with precursor miR-190b (Figure S2-D, indicated by arrows). [score:5]
Figure S2 miR-190b regulated IGF-1 protein expression. [score:4]
Furthermore, the findings that the dysregulation of miR-190b had effects on drug resistance and anti-apoptosis indicate that miR-190b could be a therapeutic target of HCC. [score:4]
Figure S3 miR-190b overexpression was correlated with prognosis in HCC patients and regulated cell viability, chemosensitivity and apoptosis in HCC cells. [score:4]
Besides HCC, up-regulation of miR-190b has been reported in miRNA profile studies of other cancers such as rectal cancer and lung cancer [43], [44]. [score:4]
Taken together, these data further confirm that miR-190b can regulate IGF-1 expression. [score:4]
of qRT-PCR confirmed that clones expressing precursor miR-190b exhibited greatly increased miR-190b expression when compared to negative controls (Figure 3A, left). [score:4]
Taken together, these results revealed that IGF-1 is a direct target of miR-190b. [score:4]
The regulatory effects of miR-190b on IGF-1 expression. [score:4]
Increased expression of miR-190 may cause decreased IGF-1 in HCC development. [score:4]
The Regulatory Effects of miR-190b on IGF-1 Expression. [score:4]
Our finding that miR-190b has a regulatory role for IGF-1 expression in human HCC supports this hypothesis. [score:4]
These results are in line with a previous report showing the up-regulation of miR-190b in rectal tumors of non-reponders to chemoradiotherapy [43]. [score:4]
IGF-1 was a direct target of miR-190b. [score:4]
As a potential regulator of IGF-1, we reasoned that expression of miR-190b might be involved in insulin resistance. [score:4]
These findings suggest a novel mechanism for the development of insulin resistance in HCC by providing the first evidence that miR-190b mediates the repression of IGF-1 expression. [score:4]
As shown in Figure S1, overexpression of miR-190b resulted in a significant decrease in IGF-1 mRNA levels after 6 hr with actinomycin D, on the contrary, IGF-1 mRNA was stable in control cells. [score:3]
The expression levels of mature miR-190b and control RNU6B were determined by qRT-PCR with the TaqMan Universal PCR Master Mix in StepOne Real-time PCR System (Applied Biosystems). [score:3]
The expression level of miR-190b was normalized by U6. [score:3]
Restoration of IGF-1 Inhibits miR-190b -mediated Insulin Resistance. [score:3]
Phosphorylation of forkhead box class O1 (FOXO1) and glycogen synthase kinase 3β (GSK3β), two downstream effectors of insulin action [24], revealed that overexpression of miR-190b critically decreased FOXO1 and GSK3β phosphorylation at Ser256 and Ser9, respectively (Figure 5A). [score:3]
Precursor miR-190b transfection significantly decreased luciferase activities whereas its inhibitor transfection increased them (Figure 2B). [score:3]
But qRT-PCR showed a modest decrease in miR-190b after transfection of the miR-190b inhibitor (Figure 3F) [22]. [score:3]
Given that IGF-1 is the main anti-apoptoic factor, we supposed that additional mechanisms induced by miR-190b were involved in this anti-apoptosis ability, independently of IGF-1 inhibition. [score:3]
TaqMan probes from Applied Biosystems were used to assess the expression of miR-190b (ID 002263) and RNU6B (ID 001093). [score:3]
In addition, upon treatment of insulin, miR-190b overexpression resulted in the diminished ability of insulin to phosphorylate GSK3β. [score:3]
To further confirm this, we analyzed the turnover of IGF-1 mRNA in miR-190b overexpressed and control cells. [score:3]
Restoration of IGF-1 inhibited miR-190b -mediated insulin resistance. [score:3]
Because the endogenous levels of miR-190b were marginally expressed in Huh7 cells, the other cell was used to conduct the loss-of-function analysis of miR-190b again. [score:3]
Overexpression of miR-190b led to further reduction of luciferase activity when the reporter construct contained IGF-1 3′UTR (Figure 2C). [score:3]
We observed that the overexpression of miR-190b increased resistance to 5-Fluorouracil (Figure S3-C). [score:3]
We examined whether the miR-190b overexpression would affect the cancer biology. [score:3]
Cells that overexpressed miR-190b produced greater amounts of glucose than did control cells (Figure 5C). [score:3]
To determine whether miR-190b affects IGF-1 expression through these putative elements, a luciferase reporter construct carrying these elements was employed. [score:3]
IGF-1 has been functionally validated as a bona fide target of miR-190b. [score:3]
We transfected the miR-190b inhibitors into HepG2 cells, which have a relatively higher basal levels of miR-190b and lower levels of IGF-1 compared to those of Huh7 cells (Figure 3E). [score:2]
Analysis of IGF-1 expression confirmed decreased IGF-1 protein levels in cells transfected with precursor miR-190b as compared to precursor controls (Figure S2-A and B). [score:2]
The WST-1 assay demonstrated a modest, but significant, decrease in cell viability upon miR-190b overexpression (Figure S3-B). [score:2]
Two reporter constructs were generated carrying mutations for each predicted miR-190b binding site. [score:2]
Figure S1 miR-190b repressed IGF-1 mRNA stability. [score:1]
We checked the relationship of miR-190b with overall survival and found that high miR-190b levels could infer a poorer overall survival prospect of HCC patients (Figure S3-A). [score:1]
To address this issue, we investigated the phosphorylation status of insulin signaling mediators by western blotting in the presence of miR-190b overexpression. [score:1]
0089446.g002 Figure 2(A) Base pairing complement suggests two putative miR-190b binding positions at 844–850 and 1752–1758 of the IGF-1 3′UTR. [score:1]
Transient transfection was also performed to clarify that IGF-1 repression was not due to clonal effects of miR-190b stable cells. [score:1]
Further, the relationship between miR-190b levels and clinicopathological features was examined. [score:1]
To validate the reliability of the microarray test, miR-190b, one of the most statistically significant miR, was selected for qRT-PCR examination. [score:1]
Huh7 cells were transiently transfected with pre-NC, pre-miR-190b, anti-NC or anti-miR-190b vectors. [score:1]
Taken together, these results indicate the critical role of miR-190b in impairing insulin signaling and promoting hepatic gluconeogenesis in HCC cells. [score:1]
Among the miR-190b stable cells, analysis of two representative subclones, namely Huh7-Pre-miR190b-6 and Huh7-Anti-miR190b-5, revealed an attenuated IGF-1 signal in Huh7-Pre-miR190b-6 cells and a moderately elevated IGF-1 signal in Huh7-Anti-miR190b-5 (Figure 3C). [score:1]
Measurement of FOXO1 translocation and glucose production revealed that the majority of FOXO1 accumulated in the nucleus upon miR-190b overexpression, whereas in control cells, FOXO1 was distributed in both nucleus and cytoplasm (Figure 5B). [score:1]
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[+] score: 139
MiR-580, miR-588 and miR-190 also downregulated TIMP-3, an endogenous inhibitor of metalloproteinases, that was recently found to be involved in the dormancy process. [score:6]
Green lines represent GFP expressing tumors while blue lines represent miR-190 over -expressing clones. [score:5]
Over -expression of DmiRs in A-GBM cells was confirmed by qRT-PCR (Information S1), and mice were injected with miR-580, miR-588, miR-190 or vector control (GFP) expressing A-GBM cells. [score:5]
In support of the data from the experimental dormancy mo dels, miR-580 and miR-190 expression was shown to correlate with disease stage in human glioma specimens. [score:5]
Inhibition of tumor growth by expression of miR-580, miR-588 or miR-190 had also been observed in osteosaroma cell lines. [score:5]
Over -expression of miR-190 in fast-growing osteosarcoma cells led to complete inhibition of osteosarcoma growth (Figure 3). [score:5]
Expression levels of genes in miR-580, miR-588 and miR-190 over -expressing A-GBM tumors were normalized to GFP-vector control. [score:5]
Hence, our data suggest that that miR-580, miR-588 and miR-190 downregulate Bv8 in a GCSF independent manner. [score:4]
MiR-190 expression led to complete (i. e., 100% inhibition, 5/5) phenotypic reversal of fast-growing osteosarcoma resulting in significant increase of overall survival (p<0.005 by log-rank test) (B). [score:4]
Among the consensus miR-580, miR-588 and miR-190 upregulated transcripts, we found two important dormancy associated genes, i. e., EphA5 and Angiomotin. [score:4]
These three DmiRs were selected based on their marked differential expression in dormant tumors; at least three out of four dormant tumors had an average of ∼ 12, 10 and 75-fold higher expression levels of miR-580, miR-588 and miR-190, as compared to the fast-growing tumors. [score:4]
It is intriguing that over -expression of a single DmiR, e. g., miR-190, was sufficient to induce a complete phenotypic reversal of fast-growing A-GBM tumors towards prolonged tumor dormancy in three out of five transfected tumors. [score:3]
It is intriguing that over -expression of a single miR, in particular miR-190, resulted in significant delay of time to tumor establishment in 40% and in sustained dormancy in 60% of GBM tumors, i. e., no detectable tumors were found by gross examination up to 140 days post injection. [score:3]
In support of the experimental data, the expression of miR-580 and miR-190 was significantly decreased with advanced tumor grade in glioma specimens. [score:3]
60% of miR-190 expressing tumors remained dormant for the whole observation period. [score:3]
Real time qRT-PCR analysis revealed significant correlation between miR-190 (p<0.0076) and miR-580 (p = 0.05) expression and tumor grade. [score:3]
In contrast, the tumor take rates were 80% (4/5) for miR-580, 75% (3/4) for miR-588 and only 40% (2/5) in miR-190 over -expressing tumors (Table 1). [score:3]
Unfortunately, the knowledge of the function and potential gene targets of miR-580, miR-588 and miR-190 is very limited and their contribution to cancer progression is unknown. [score:3]
The growth dynamics of single tumors within the GFP-vector-control and miR-190 expressing tumors are presented in the Information S1. [score:3]
Using qRT-PCR the efficacy of DmiR transfection was confirmed by analyzing their expression levels in miR-580, miR-588 or miR-190 vs. [score:3]
Moreover, miR-190 expression led to complete phenotypic reversal in 100% of fast-growing A-Osteosarcoma. [score:3]
Moreover, we tested the expression of miR-190 in a fast-growing A-Osteosarcoma mo del. [score:3]
As shown in Figure 1 C–D, the expression levels of miR-580 and miR-190 decreased with advanced tumor grade. [score:3]
The expression level of miR-580, miR-588 and miR-190 was detected in human glioma specimens (C–E). [score:3]
Expression of miR-580, miR-588, miR-190 as well as the control-GFP-vector neither blocks cell proliferation nor enhances cell death even in-vitro at hyperconfluence state (after 144h) as determined by caspase 3/7 activity (Figure 2C). [score:3]
Average tumor volume of parental tumor (labeled in red line) n = 11, cells infected with GFP only control vector (n = 9), miR-580 (n = 5), miR-588 (n = 4), and miR-190 (n = 5) expressing A-GBM tumors. [score:3]
To prove this hypothesis, we reconstituted the expression of miR-580, miR-588 or miR-190 in fast-growing A-GBM tumors. [score:3]
Complete phenotypic reversal after miR-190 expression in fast-growing osteosarcoma. [score:3]
During the observation period of >120 days, no tumor was detected by gross examination in miR-190 expressing osteoscaroma (0/5), whereas the vector control GFP osteosarcoma exhibited 100% tumor take (5/5). [score:3]
Of note, the median survival time of the mice with miR-190 expressing tumors exceeded the observation period. [score:3]
The average tumor dormancy period, i. e., the time until tumors became detectable by gross examination, was increased to ∼ 100 days by over -expression of a single DmiR (e. g., miR-580 or miR-190). [score:3]
Over -expression of miR-580, miR-588 and miR-190 in fast-growing angiogenic glioblastoma. [score:3]
We detected more than 210-fold higher expression levels of miR-190 in dormant vs. [score:3]
To test potential dormancy promoting functional effects of the identified DmiRs, lentiviral vectors encoding miR-580, miR-588 or miR-190 were used to reconstitute their expression in fast-growing angiogenic T98G human glioblastoma multiforme cells (A-GBM). [score:3]
miR-190 (n = 5) expressing angiogenic fast-growing “A-Osteosarcoma” (A). [score:3]
MiR-190 expression in osteosarcoma mo del. [score:2]
Confirmation of miR-580 and miR-190 regulation in an independent tumor set. [score:2]
The regulation of miR-580 and miR-190 was further confirmed in a second independent set of dormant vs. [score:2]
To examine the regulation patterns of the identified DmiRs in primary human tumor tissue, the expression levels of miR-580, miR-588 and miR-190 in tissue specimens of glioma patients were investigated. [score:2]
Tumor growth was compared between GFP and miR-190 over -expressing clones of fast growing glioblastoma (A-GBM). [score:2]
For all subsequent confirmatory and functional validation studies, the top three dormancy -associated miRs miR-580, miR-588 and miR-190– were used. [score:1]
Together, these data support the proposed potent dormancy promoting effect of miR-190. [score:1]
MicroRNA-190 was the most effective dormancy promoting DmiR in our GBM mo del. [score:1]
Statistical significance was reached for miR-190 (p<0.03) and miR-580 (p = 0.05), respectively, by log-rank test. [score:1]
In line with this observation, overall survival was significantly prolonged in miR-190 vs. [score:1]
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[+] score: 28
With regards to oncogenesis mechanism, it should be noted that the FOXP2 transcript is a bona fide target of miR-190, a microRNA lying within an intron of, and concomitantly expressed with, the cytoskeleton -associated protein TALIN2 (TLN2) - with both genes being down-regulated in advanced prostate cancer [143]. [score:8]
Noticeably, in glioblastomas and osteosarcomas in in vivo mo dels of human cancer in immune-compromised mice, up-regulation of miR-190 led to prolonged tumor dormancy [55]. [score:4]
One, miR-190, has been reported to be up-regulated in both gastric cancer biopsies and in one established gastric cancer cell line [10]. [score:4]
Conversely, up-regulated miR-190 has been reported in a variety of conditions such as bladder cancer, breast cancer, lung cancer, liver cancer, and colorectal cancer, as well as in bronchial epithelial cell cancerization induced by arsenic [56- 61]. [score:4]
One assumption is thus that elevated miR-190 might lead to reduced target FOXP2 transcripts, as observed in established cell lines [55]. [score:3]
Altogether these observations in diverse oncogenic conditions point to the susceptibility of FOXP2 expression levels to the activity of miR-190, which in some cases has been associated with oncogenic initiation. [score:3]
One frequent candidate is the miR-190. [score:1]
As reported in other sections, miR-190 is often found associated with tumorigenic conditions. [score:1]
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[+] score: 17
Of the differentially expressed miRNAs, miR-185, miR-150, miR-194, and miR-363 were downregulated in individuals with 22q11DS as compared to TD controls and miR-208, miR-190, and miR-1 were upregulated. [score:8]
In the presented study we observed an increased expression of miR-208 and miR-190 in 22q11DS compared to controls; interestingly a significant up-regulation of these miRNAs were reported in patients with myocardial infarction [69] suggesting their contributing role in cardiac disease. [score:7]
Several miRNAs have been implicated in cardiogenesis and heart development including miR-1, miR208 and miR-190 [69]– [71]. [score:2]
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[+] score: 17
The predicted targets of hsa-miR-190b are enriched in some cancer-related pathway (Supplementary Table 5), such as signaling pathways regulating pluripotency of stem cells (p-value = 0.058), cell adhesion molecules (CAMs) (p-value = 0.058) 25 and AMPK signaling pathway (p-value = 0.042) 26. [score:4]
In MCF-7 docetaxel-resistant breast cancer cells, the miRNA set containing miR-190b was down-regulated 24. [score:4]
We next explored hsa-miR-190b targets, with only predicted ones being found (Supplementary Table 5). [score:3]
We found hsa-miR-190b be over-expressed in ER+ tumors, and HER2+ tumors among ER− cancers. [score:3]
This, on one hand, offers the evidence supporting the differentiation hierarchical structure underlying breast cancer heterogeneity and, on the other hand, indicates that the genes under hsa-miR-190b regulation might unveil the key network or pathways driving such a differentiation. [score:2]
The fact that hsa-miR-190b is firstly responsive to the hormonal receptor ER and secondarily to the growth receptor HER2, is consistent with the hierarchical structure in our constructed decision tree. [score:1]
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[+] score: 16
Developmental stage of O. felineus miRNAs AdultNoEggs & Adult+Eggs & Metacercaria let-7, miR-1, miR-2(a,b,c,d,e), miR-36, miR-71(a,b), miR-124, miR-125, miR-133, miR-190 AdultNoEggs & Adult+Eggs bantam, miR-281(miR-46 family) AdultNoEggs & Metacercaria miR-7 Metacercaria miR-10 Candidate sequences for novel miRNAs (S4 Table) were selected from reads without matches to miRBase sequences after mapping them to the C. sinensis genome and processing the genomic fragments encompassing the resultant hits through the secondary structure filter (see ). [score:2]
Developmental stage of O. felineus miRNAs AdultNoEggs & Adult+Eggs & Metacercaria let-7, miR-1, miR-2(a,b,c,d,e), miR-36, miR-71(a,b), miR-124, miR-125, miR-133, miR-190 AdultNoEggs & Adult+Eggs bantam, miR-281(miR-46 family) AdultNoEggs & Metacercaria miR-7 Metacercaria miR-10Candidate sequences for novel miRNAs (S4 Table) were selected from reads without matches to miRBase sequences after mapping them to the C. sinensis genome and processing the genomic fragments encompassing the resultant hits through the secondary structure filter (see ). [score:2]
Alignment of miR-190 precursors in the context of corresponding introns. [score:1]
The intronic nature of the miR-190 gene has been described for many animals [36, 45, 76]. [score:1]
Therefore, we could classify this miR-190 as intronic [72]. [score:1]
miRNA Genomes C. sinensis S. mansoni S. japonicum bantam + + + let-7 + + + miR-1 + + − miR-2a + + + miR-2b + + + miR-2c + + + miR-2d + + + miR-2e + + + miR-7 + + + miR-10 + + + miR-36a + + + miR-36b + − − miR-281 + + + miR-71a + + + miR-71b + + + miR-124 + + + miR-125 − + + miR-133 + + + miR-190 + + + Mapped miRNA is designated by plus; unmapped—by minus. [score:1]
The present analysis corroborates the classification of the miR-190 gene as intronic within the talin gene. [score:1]
The ortholog search for the miRNAs of the three opisthorchiids yielded 19 conserved miRNAs belonging to 13 families (bantam, let-7, miR-1, miR-2, mir-7, miR-10, miR-36, miR-46, miR-71, miR-124, miR-125, miR-133, and miR-190) (Fig 2A, Table 1, S3 Table). [score:1]
The mapping of miR-190, which was also identified in the three opisthorchiid species, to the available flatworm genomic sequences showed that this miRNA is located in an intron of the gene encoding the talin protein. [score:1]
High conservation of the structural (and maybe functional) association between miR-190 and the talin protein in platyhelminths appears very interesting and is worthy of further elucidation. [score:1]
miR-190 is an intronic miRNA. [score:1]
The alignments of some miRNAs (two miR-71/ miR-2 clusters, miR-1, miR-133, and miR-190) with sequences of these miRNAs orthologs (obtained from S. mediterranea, G. salaris, S. mansoni, S. japonicum, E. granulosus, E. multilocularis, H. microstoma and T. solium genomes) were performed using the program CLUSTALW [68]; miRNA sequences of T. solium, namely miR-1, miR-2b, miR-2c, miR-71, miR-133, miR-190, were obtained by homology search of these miRNAs in T. solium genome (http://www. [score:1]
Designations are the same as in Fig 3. The mapping of miR-190, which was also identified in the three opisthorchiid species, to the available flatworm genomic sequences showed that this miRNA is located in an intron of the gene encoding the talin protein. [score:1]
Structures of Trematoda and Cestoda talin genes with intronic miR-190. [score:1]
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[+] score: 14
For example, TE miRNA miR-190 can target Socs36E, a negative regulator of JAK/STAT signaling [29], suggesting miR-190 may enhance tumorigenesis through activating JAK/STAT signaling. [score:4]
However, overexpression of these miRNAs (e. g. bantam, miR-190, miR-2a-1, miR-2b-2) individually does not display tumorigenic phenotypes in the Drosophila wing disc (Supplementary Figure 4). [score:3]
Overexpression of miR-190 enhances proliferation and malignant transformation through activation of Akt signaling [35]. [score:3]
Tumor-enhancing miRNAs, mir-10 (C-C’’), mir-190 (D-D’’), mir-277 (E-E’’), and mir-2a-1, 2b-2 (F-F’’) were expressed in the dpp>lgl -RNAi background individually, and induced tumors. [score:3]
In addition to miR-10 discussed above, miR-190 has also been mechanistically involved in various human cancers. [score:1]
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[+] score: 13
miR-190b had an almost discrete binary expression mode with higher expression in the luminal-A/B subtypes than in the basal-like/ERBB2-enriched subtypes (TNoM p<4E-15). [score:5]
Expression profiles (signal intensities) of miR-9*, miR-29c and miR-190b ordered by subtypes. [score:3]
Figure S1 Expression profiles of miR-9*, miR-29c and miR-190b in subtypes. [score:3]
Among the prominently down regulated miRNAs in basal-like tumors were representatives of the miR-29 family (TNoM p<7E-12) along with miR-190b (TNoM p<2E-10) (Figure S1B-C). [score:2]
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[+] score: 13
We also identified EB upregulated miRNAs that have not been previously reported such as miR-130a, miR-301a, and miR-135, miR-190, miR-30c, and miR-30e. [score:4]
The expression of miR-106a, miR-106b, miR-17-5p, miR-92, miR-93, miR-190, miR-20a and miR-130 were highest in EB (panel B). [score:3]
The expression of miR-106a, miR-106b, miR-17-5p, miR-92, miR-93, miR-130a, miR-20a and miR-190 were much higher in EB than in either hES cells or adult cells (Figure 6, panel B). [score:3]
For miR-106b, miR-92, miR-93, miR-130a and miR-190, the difference in their expression between EB and hES cells and between EB and adult cells were significant (P < 0.05). [score:3]
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[+] score: 9
miR222 targets the PPP2R2Asubunit of PP2A in HCC to disrupt cell motility and miR-190 inhibits PHLPP expression and promotes carcinogenic transformation of bronchial cells suggesting that the AKT pathway is a prominent target of miRNA activity [148, 149]. [score:9]
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[+] score: 9
Dre-miR-146a exhibited the largest effect size (6.73-fold upregulation) in MC-RR exposed zebrafish embryos relative to controls, whereas the expression of dre-miR-190b showed the largest downregulation (4.61-fold). [score:9]
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[+] score: 8
Expression of miR-1284, miR-942, miR-630, and miR-190b. [score:3]
MicroRNAs miR-190b, miR-630, miR-942, and miR-1284, the most frequent constituents of the classifiers generated in the current study, are not differentially expressed between cases and controls in the data-sets of either Keller, et al. or Leidinger, et al. as per the limma -based test used in the current study. [score:3]
MicroRNAs miR-190b, miR-942 and miR-1284 were present in all of them. [score:1]
Overall, the two classification methods, SVM and TSP, identified four microRNAs (miR-190b, miR-630, miR-942, and miR-1284) that were present in a majority of the classifiers that were generated in the cross-validation analyses. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-190a, hsa-mir-580, hsa-mir-588
Recently, miR-34a was reported to negatively modulate chondrogenesis by targeting EphA5 in chick limb mesenchymal cells [61], whereas antiangiogenic and dormancy-promoting molecules including EphA5 were reported to be upregulated by expression of dormancy -associated miR-580, miR-588, and miR-190 [37]. [score:8]
[1 to 20 of 1 sentences]
[+] score: 7
We selected 12 miRNAs: miR-9, miR-19b, miR-27b, miR-92a, miR-140-5p, miR-190, miR-200a, let-7a, miR-129-5p, miR-582-5p, miR-892a, and miR-1237 (Figure  1) and tested whether they downregulate FOXP2 expression in cell culture systems. [score:6]
In contrast, miR-27b, miR-92a, miR-190, and miR-1237 did not repress luciferase activity whether the reporter constructs contained a FOXP2 3′ UTR or not (Figure  3A). [score:1]
[1 to 20 of 2 sentences]
[+] score: 7
The comparison between control- and MPA -treated cells revealed that 16 miRNAs were significantly modulated by more than two-fold (P < 0.05, Figure 1A), nine miRNAs were upregulated (miR-191*, miR-17*, miR- 470*, miR-451, miR-702, miR-434-3p, miR-493, miR-23a* and miR-485*) and seven were downregulated (miR-378*, miR-376a, miR-224, miR-190b, miR-16, miR-410 and miR-197) (Figure 1B). [score:7]
[1 to 20 of 1 sentences]
[+] score: 6
Other miRNAs from this paper: mmu-mir-190a, hsa-mir-190a, mmu-mir-190b
Yu Y Zhang D Huang H Li J Zhang M Wan Y Gao J Huang C NF-kappaB1 p50 promotes p53 protein translation through miR-190 downregulation of PHLPP1Oncogene 2013 37. [score:6]
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[+] score: 6
Hsa-miR-190b show sequence identify of 79% (with blast similarity score = 28.3, E-value = 2E-05) and 77% (with blast similarity score = 76.1, E-value = 2E-18) with sly-miR-171a (tomato) and miR-190a (human), respectively. [score:1]
In Fig 2, we illustrated the sequences conservation using a phylogenetic tree built on the precursor sequences of miR-190 and -171 families. [score:1]
Phylogenetic tree of miR-190/171 family and sequence alignments of hsa-miR-190a/b and sly-MIR171a. [score:1]
0140587.g002 Fig 2 (A) Phylogenetic tree of miR-190/171 family based on the 162 precursor sequences from 89 species, where three major clusters are formed for miR-190a, miR-190b, and miR-171. [score:1]
Specifically, human miRNA, hsa-miR-190b, show sequence identify of 79% and 77% with sly-miR-171a (tomato) and miR-190a (human), respectively (alignments shown in Fig 2B). [score:1]
It showed, among three miRNA gene clusters (miR-190a, miR-190b, miR-171), human miR-190a and -190b are close to many animal species, e. g. cow and mouse, within their respective clusters. [score:1]
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[+] score: 6
Our results in the two cell lines agree with previously published data on the upregulation of MIR93, MIR95, MIR135B, MIR181C, MIR181D, MIR182, MIR183, MIR190, MIR196B and MIR203, and downregulation of MIR20A and MIR29C in pancreatic intraepithelial neoplasms (PanIns) or pancreatic adenocarcinomas (PDACs) as compared to normal pancreatic tissue [34- 36]. [score:6]
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[+] score: 6
In another report, Jia et al firstly reported that an increased expression of miR-190 led to downregulation of FOXP2 in GC cells [145]. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
Microarray profiling studies showed reduction in miRNAs expression specific of HCV and HBV -associated cases: down-regulation of miR-190, miR-134, and miR-151 occurs in HCV cases, and of miR-23a, miR-142-5p, miR-34c, in HBV cases (Ura et al., 2009). [score:6]
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[+] score: 5
Beezhold K. Liu J. Kan H. Meighan T. Castranova V. Shi X. Chen F. miR-190 -mediated downregulation of PHLPP contributes to arsenic -induced Akt activation and carcinogenesisToxicol. [score:4]
Moreover, induction of miR-190 can accelerate proliferation of human bronchial epithelial cells in the process of arsenite -induced carcinogenesis [20]. [score:1]
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[+] score: 5
The miRNA signatures generated for ER status (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), for PR status (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and for HER2/ neu status (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) include miRNAs that have previously been identified as dysregulated in breast cancer and other cancers [7, 9, 37- 43] and involved in the regulation of cell functions such as growth, apoptosis, migration and invasion [38, 42, 43]. [score:3]
The ER signature consisted of six miRNA transcripts (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), and discriminated cases correctly with a median accuracy of 100% when classifying between ER -positive and ER -negative phenotypes. [score:1]
Stepwise ANN analysis identified predictive miRNA signatures corresponding with oestrogen (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), progesterone (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and HER2/ neu (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) receptor status. [score:1]
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[+] score: 5
Previous study focused on the involvement of this miRNA in the development of tolerant to μ-opioid receptor agonists with NEUROD1 (a neural differentiation marker) as the direct target for mir-190 43. [score:5]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-215, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519c, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-421, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
Similar global profiling approaches have revealed other miRNAs may target the nutrient sensing pathways; levels of miR-190b were found to be elevated in samples from patients with hepatocellular carcinoma, and were demonstrated to be associated with low serum IGF1 expression and insulin resistance in these patients [71]. [score:5]
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[+] score: 5
MicroRNAs miR-187 (previously identified to be induced by influenza A virus [26]), miR-147b, miR-190b, miR-874, and the miR-449 family (miR-449a, miR-449b, and miR-449c) were all validated as highly regulated by influenza A virus infection (Figure 2). [score:2]
Transfections were performed using the following miRNA specific mimics at a final concentration of 50nM: miR-141, miR-147b, miR-190b, miR-199a-5p, miR-374b, miR-449b, miR-512-5p, miR-518b, miR-874, and miR-1263 (Thermo Scientific/Dharmacon). [score:1]
Ten highly inducible miRNAs (miR-141, miR-147b, miR-190b, miR-199a-5p, miR-374b, miR-449b, miR-512-5p, miR-518b, miR-874, and miR-1263) were used in this experiment and divided randomly into two groups of 5 for analysis: one group (G1) consisted of miR-141, miR-374b, miR-449b, miR-518b, and miR-1263, and the other group (G2) consisted of miR-147b, miR-190b, miR-199a-5p, miR-512-5p, and miR-874 (Figure 3A). [score:1]
0076560.g003 Figure 3 (A) A549 cells were mock infected, infected with A/WSN/33 (5 pfu/cell), or infected after transfection with an equimolar mixture of miRNAs (50nM final concentration) that included either hsa-miR-141, hsa-miR-374b, hsa-miR-449b, hsa-miR-518b, and hsa-miR-1263 (G1), or hsa-miR-147b, hsa-miR-190b, hsa-miR-199a-5p, hsa-miR-512-5p, and hsa-miR-874 (G2). [score:1]
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[+] score: 4
Colorectal cancer cell lines with KRAS mutations showed an over -expression of miR-9, miR-9*, miR-95, miR-148a, miR-190 and miR-372, in relation to the human normal colon cell line. [score:4]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-190a, hsa-mir-190a, mmu-mir-190b
In addition, As [3+] is able to induce the biogenesis of microRNA-190 (miR-190) that is responsible for the down-regulation of PHLPP. [score:4]
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[+] score: 3
Also, Patnaik and colleagues identified microRNA expression profiles of whole blood in LAD, and showed that microRNAs miR-190b, miR-630, miR-942, and miR-1284 were the most frequent constituents of the classifiers [21]. [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-18a, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-200b, mmu-mir-203, mmu-mir-204, mmu-mir-205, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-203a, hsa-mir-204, hsa-mir-205, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-100, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-375, mmu-mir-375, hsa-mir-335, mmu-mir-335, mmu-mir-133a-2, hsa-mir-424, hsa-mir-193b, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-518f, hsa-mir-518b, hsa-mir-517a, hsa-mir-519d, hsa-mir-516b-2, hsa-mir-516b-1, hsa-mir-517c, hsa-mir-519a-1, hsa-mir-516a-1, hsa-mir-516a-2, hsa-mir-519a-2, hsa-mir-503, mmu-mir-503, hsa-mir-642a, mmu-mir-190b, mmu-mir-193b, mmu-mir-1b, hsa-mir-203b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The luminal subtypes of breast cancer appear to have elevated expression of miR-190b, while basal-like tumors have higher levels of miR-18a/b, miR-9 and the miR-17-92 family and lower levels of miR-29 and miR-190b [55]. [score:3]
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[+] score: 3
Similarly, overexpression of miR190 in C4-2 and 22Rv1 cells decreased the protein levels of AR and YB-1 (Fig. 2g,i). [score:3]
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[+] score: 3
miR-190b negatively contributes to the trypanosoma cruzi-infected cell survival by repressing PTEN protein expression. [score:3]
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[+] score: 3
Both the 3p and 5p miRNAs for miR-190 and miR-340 were affected by the deletion of EBER1, indicating that the promoters driving expression of the primary miRNA transcripts were affected (Fig. 2B), consistent with a recent report on miR-190 (9). [score:3]
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[+] score: 3
For three other miRNAs—mir-190, mir-281 and mir-8451—reported to be conserved among the Bilateria, Protostomia and Platyhelminthes, respectively [10], no representatives were detected in S. haematobium. [score:1]
To test this hypothesis, we assessed whether mature and precursor sequences of sma-mir-190, sma-mir-281 and sma-mir-8451 were homologous to any S. haematobium miRNAs identified using a less stringent (blastn -task “blastn-short”) approach [43]. [score:1]
However, transcription in adult stages has been reported for mir-190 in both S. japonicum [13, 21] and S. mansoni [10], and for mir-281 in S. mansoni [10], suggesting that homologs of these miRNAs were not identified here in S. haematobium due to the stringency with which miRDeep2 defines high-confidence homologs, requiring an exact nucleotide match for positions 2–8 (‘seed’) of the mature sequence. [score:1]
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[+] score: 2
Pathway name KO identifier microRNA Toll-like receptor signaling pathway ko04620 tca-miR-1175-5p Fc gamma R -mediated phagocytosis ko04666hme-miR-190 cqu-miR-1175-5paae-miR-1175-5p tca-miR-1175-5pisc-miR-276 Chemokine signaling pathway ko04062 tca-miR-1175-5p Leukocyte transendothelial migration ko04670 isc-miR-276 tca-miR-71-5p Apoptosis ko04210 hme-miR-190 New Zealand rabbits were provided by the Laboratory Animal Center of Sichuan Agricultural University (Ya’an, China). [score:1]
Pathway name KO identifier microRNA Toll-like receptor signaling pathway ko04620 tca-miR-1175-5p Fc gamma R -mediated phagocytosis ko04666hme-miR-190 cqu-miR-1175-5paae-miR-1175-5p tca-miR-1175-5pisc-miR-276 Chemokine signaling pathway ko04062 tca-miR-1175-5p Leukocyte transendothelial migration ko04670 isc-miR-276 tca-miR-71-5p Apoptosis ko04210 hme-miR-190 A total of 47,866,350 raw sequence reads were generated from the starved S. scabiei with 43,425,649 clean reads after filtering. [score:1]
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[+] score: 2
We confirmed 90% of the deregulated miRNAs (Figure 1); only miR-190 was not changed (data not shown). [score:2]
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[+] score: 2
The topological parameters of these 14 nodes (Table 7 ) showed that the highly connected nodes (hsa-miR-190, hsa-miR-155, hsa-miR-338-3p) also have very high BC value and low eccentricity value. [score:1]
Previous studies have established a link between hsa-miR-190 and the aggressive phenotype of neuroblastoma [64]. [score:1]
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[+] score: 2
As [III ]can also activate AKT independently of PI3K, both through STAT3 and/or induction of miR-190. [score:1]
Arsenic -induced activation of AKT may be also associated with its ability to cause the induction of miR-190. [score:1]
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[+] score: 2
In addition, miR-190 not detectable by microarray was shown to be differentially regulated by full-length HBx and HBxΔ35 (Figure 3B), presumably due to superior sensitivity of real-time PCR. [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-30a, hsa-mir-32, hsa-mir-33a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-147a, hsa-mir-34a, hsa-mir-187, hsa-mir-204, hsa-mir-205, hsa-mir-200b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-138-2, hsa-mir-142, hsa-mir-144, hsa-mir-125b-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-190a, hsa-mir-200c, hsa-mir-155, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-365b, hsa-mir-328, gga-mir-33-1, gga-mir-125b-2, gga-mir-155, gga-mir-17, gga-mir-148a, gga-mir-138-1, gga-mir-187, gga-mir-32, gga-mir-30d, gga-mir-30b, gga-mir-30a, gga-mir-30c-2, gga-mir-190a, gga-mir-204-2, gga-mir-138-2, gga-let-7d, gga-let-7f, gga-mir-146a, gga-mir-205b, gga-mir-200a, gga-mir-200b, gga-mir-34a, gga-mir-30e, gga-mir-30c-1, gga-mir-205a, gga-mir-204-1, gga-mir-23b, gga-mir-142, hsa-mir-449a, hsa-mir-489, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-33b, hsa-mir-449b, gga-mir-146b, gga-mir-147, gga-mir-489, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-144, gga-mir-460a, hsa-mir-147b, gga-mir-22, gga-mir-460b, gga-mir-1662, gga-mir-1684a, gga-mir-449c, gga-mir-146c, gga-mir-449b, gga-mir-2954, hsa-mir-548aa-1, hsa-mir-548aa-2, 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-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, gga-mir-365b, gga-mir-33-2, gga-mir-125b-1, gga-mir-190b, gga-mir-449d, gga-mir-205c
Evidences indicated the miRNAs are crucial regulators in PH induced by hypoxia, and miR-190, miR-328 and miR-138 all help to promote pulmonary vascular remo deling [8– 10]. [score:2]
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[+] score: 2
Thirteen mRNA were specifically related to homozygous/heterozygous status of KIT mutation: miR-518f, miR-331, miR-628, miR-145, miR-139, miR-335, miR-526b, miR-190, miR-548c, miR-202, miR-339, miR-203, and miR-301b (Anova test p<0.05). [score:2]
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[+] score: 2
Another group of 17 miRNAs (hsa-miR-575, hsa-miR-155, hsa-miR-26b, hsa-miR-200a, hsa-miR-200b, hsa-miR-141, hsa-miR-200c, hsa-miR-190b, hsa-miR-492, hsa-miR-640, hsa-miR-196a, hsa-miR-29c, hsa-miR-93, hsa-miR-193a-3p, hsa-miR-191, hsa-miR-26a, hsa-miR-182) showed significantly higher expression in the major cluster compared with the other miRNAs (fold change ≥ 1.5) (Figure 2, bottom red box). [score:2]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-190a
In human bronchial epithelial cells or lung cancer cells, we had shown that As [3+] is able to activate protein kinase Akt through either inducing miR-190 or initiating the signaling cascade from JNK to STAT3 that contributes to Akt -dependent EZH2 phosphorylation, cell transformation and/or migration [7– 10]. [score:1]
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Of these 7 miRNAs, 2 (hsa-mir-139, hsa-mir-326) were negatively correlated with survival, while the other 5 (miR-101-2, miR-182, miR-183, miR-190, hsa-miR-944) were protective. [score:1]
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In the remaining 46 miRNAs with a corresponding Affymetrix U133A probe for their pri-miRNA transcripts, the ratio of miRNA to host mRNA was significantly lower for two pri-miRNAs (primary transcripts for miR-218, p = 0.021, and miR-9, p = 0.006) and significantly higher for five (miR-482, p = 0.015; miR-190, p = 0.018; miR-105, p = 0.02; miR-148b, p = 0.027; miR-218, p = 0.02). [score:1]
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In the single miRNA analysis three microRNA were found to be significant in both datasets (hsa-miR-105, hsa-miR-190, hsa-miR-433), however, in the single gene analysis we could not find even one gene that stratify prognosis robustly in both datasets. [score:1]
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For the ‘meningioma’ query, miRCancer retrieved 4 miRNAs (hsa-mir-128, hsa-mir-200a, hsa-mir-224, hsa-mir-335) and miRiaD retrieved 4 additional miRNAs (hsa-mir-145, hsa-mir-190, hsa-mir-219, and hsa-mir-29). [score:1]
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Other miRNAs from this paper: hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, dme-mir-1, dme-mir-8, dme-mir-11, hsa-mir-34a, hsa-mir-210, dme-mir-184, dme-mir-275, dme-mir-92a, dme-mir-276a, dme-mir-277, dme-mir-33, dme-mir-281-1, dme-mir-281-2, dme-mir-34, dme-mir-276b, dme-mir-210, dme-mir-92b, dme-bantam, dme-mir-309, dme-mir-317, hsa-mir-1-2, hsa-mir-184, hsa-mir-190a, hsa-mir-1-1, hsa-mir-34b, hsa-mir-34c, aga-bantam, aga-mir-1, aga-mir-184, aga-mir-210, aga-mir-275, aga-mir-276, aga-mir-277, aga-mir-281, aga-mir-317, aga-mir-8, aga-mir-92a, aga-mir-92b, hsa-mir-92b, hsa-mir-33b, dme-mir-190, dme-mir-957, dme-mir-970, dme-mir-980, dme-mir-981, dme-mir-927, dme-mir-989, dme-mir-252, dme-mir-1000, aga-mir-1174, aga-mir-1175, aga-mir-34, aga-mir-989, aga-mir-11, aga-mir-981, aga-mir-1889, aga-mir-1890, aga-mir-1891, aga-mir-190, aga-mir-927, aga-mir-970, aga-mir-957, aga-mir-1000, aga-mir-309, cqu-mir-1174, cqu-mir-281-1, cqu-mir-1, cqu-mir-275, cqu-mir-957, cqu-mir-277, cqu-mir-252-1, cqu-mir-970, cqu-mir-317-1, cqu-mir-981, cqu-mir-989, cqu-mir-1175, cqu-mir-276-1, cqu-mir-276-2, cqu-mir-276-3, cqu-mir-210, cqu-mir-92, cqu-mir-190-2, cqu-mir-190-1, cqu-mir-1000, cqu-mir-11, cqu-mir-8, cqu-bantam, cqu-mir-1891, cqu-mir-184, cqu-mir-1890, cqu-mir-980, cqu-mir-33, cqu-mir-2951, cqu-mir-2941-1, cqu-mir-2941-2, cqu-mir-2952, cqu-mir-1889, cqu-mir-309, cqu-mir-252-2, cqu-mir-281-2, cqu-mir-317-2, aga-mir-2944a-1, aga-mir-2944a-2, aga-mir-2944b, aga-mir-2945, aga-mir-33, aga-mir-980
quinquefasciatus miRNAs, miR-317, miR-252, miR-276, miR-190, miR-981, and miR-2944, arise from at least two possible hairpin precursors (Table 2). [score:1]
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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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Similarly, stepwise artificial neural networks analysis revealed predictive miRNA signatures (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218) corresponding to oestrogen receptor status in breast cancer [39]. [score:1]
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Second, they have wide differences in GC content, ranging from 23% (miR-190) to 68% (miR-328). [score:1]
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