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43 publications mentioning hsa-mir-190a

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

[+] score: 290
miR-190a is known to be downregulated in aggressive neuroblastoma (NBL), and overexpression of miR-190a leads to inhibition of tumor growth and prolonged dormancy periods in fast growing tumors 8. Recent study showed that miR-190a is involved in estrogen receptor (ERα) signaling, causing inhibition of breast tumor metastasis 9. Androgen has been shown to repress the expression of miR-99a/let7c/125b-2 cluster through AR 23. [score:12]
Based on these observations, we hypothesized that miR-190a inhibits AR transactivation and expression through direct downregulation of YB-1 expression. [score:11]
AR/miR-190a/YB-1 signaling forms an auto-regulatory negative feedback loop in prostate cancer, where androgen/AR inhibits miR-190a expression through direct binding to the ARE in the miR-190a promoter, and miR-190a inhibits AR expression and activity through binding 3′-UTR of YB-1 gene. [score:11]
Based on AR/miR-190a/YB-1 negative feedback loop, we speculate that, at the CSPC stage, activation of AR upon androgen binding inhibits miR-190a expression, while the androgen ablation promotes the expression of miR-190a, further causing inhibition of AR expression and activation. [score:11]
Furthermore, miR-190a suppressed AR expression and transactivation through targeting YB-1. This study revealed a novel mechanism by which miR-190a regulates AR signaling through targeting YB-1 in the development of prostate cancer. [score:11]
As shown in Fig. 6d–h, tumors with overexpressed miR-190a had reduced expression of AR, YB-1 and Ki-67, and increased CDKN1A, suggesting that overexpression of miR-190a inhibited prostate tumor growth in vivo. [score:9]
MiR-190a -mediated suppression of AR expression and transactivation requires miR-190a binding to the 3′-UTR of YB-1 geneOur previous study demonstrated that miR-190a inhibited YB-1 and AR expression. [score:9]
As shown in Fig. 4b,c, overexpression of miR-190a inhibited YB-1 wild-type, but not mutant luciferase reporter activities in LNCaP and 22Rv1 cells, indicating that miR-190a specifically targets YB-1 through direct 3′-UTR binding. [score:8]
miR-190a inhibits YB-1 and AR expression and specifically targets YB-1 through direct 3′-UTR binding. [score:8]
Herein, we provided evidence from human prostate cancer tissues showing that endogenous miR-190a expression is inversely correlated with PSA levels, and that patients with higher miR-190a expression in their tumors have improved disease-free survival. [score:7]
miR-190a inhibited AR expression, while YB-1 knockdown abolished the miR-190a -mediated repression (Fig. 4d). [score:6]
Taken together, these results suggest that androgen inhibits miR-190a expression through direct binding to the half-site of ARE in miR-190a promoter. [score:6]
Furthermore, overexpression of miR-190a with simultaneous depletion of AR in C4-2 cells inhibited cell proliferation and colony formation in the presence of endogenous AR (Fig. 5b,d), while AR knockdown alleviated the miR-190a -mediated repression. [score:6]
Importantly, miR-190a, a tumor suppressor miRNA, was newly identified miRNA that was remarkably downregulated in LNCaP/DHT compared with LNCaP. [score:5]
Our previous study demonstrated that miR-190a inhibited YB-1 and AR expression. [score:5]
Overexpression of miR-190a decreased LNCaP cell growth potential in the presence of DHT, while androgen-deprivation abolished miR-190a -mediated inhibition of cellular proliferation (Fig. 5a). [score:5]
MiR-190a inhibits prostate tumor growth in vivoTo investigate the role of miR-190a in inhibition of prostate cancer growth in vivo, we established C4-2 cells stably expressing miR-190a or miR-SC. [score:5]
This data suggested that miR-190a -mediated repression of AR protein levels is dependent on the presence of YB-1. Consistent with this observation, overexpression of YB-1 in LNCaP cells rescued the loss of AR expression induced by miR-190a (Fig. 4e). [score:5]
Herein, we demonstrate that miR-190a regulates AR signaling through targeting YB-1, a known AR regulator. [score:5]
MiR-190a -mediated suppression of AR expression and transactivation requires miR-190a binding to the 3′-UTR of YB-1 gene. [score:5]
Patients with tumors exhibiting high miR-190a expression levels (n = 18) associated with significantly lower disease-free survival (p = 0.035) (Fig. 7c). [score:5]
Luciferase reporter assays were further performed to determine whether miR-190a -mediated suppression of AR activity requires YB-1. As shown in the Fig. 4f, overexpression of miR-190a decreased androgen -induced PSA-Luc activity, while transient transfection of LNCaP cells with knockdown YB-1 abolished the repression. [score:5]
Our study showed that miR-190a inhibited YB-1 expression. [score:5]
At the CRPC stage, long-term androgen deprivation therapy leads to abnormal activation of AR independent of androgen stimulus, which decreases miR-190a expression, further enhancing YB-1 expression and activation. [score:5]
Overexpression of miR-190a in LNCaP, C4-2 and 22Rv1 cells inhibited cell growth (Fig. 5a–e, Supplemental Fig. 2a,b). [score:5]
Collectively, these observations indicate that miR-190a is downregulated by AR activation. [score:4]
MiR-190a inhibits AR expression and transactivation. [score:4]
MiR-190a inhibits AR expression and its trans-activation. [score:4]
As shown in Fig. 1c,d, shRNA -mediated knockdown of AR in LNCaP cells induced increase in miR-190a levels, whereas overexpression of AR in PC3 cells significantly reduced miR-190a levels. [score:4]
As shown in Fig. 2a,f,h, the expression of miR-190a in these cell lines were higher than in scramble control cells. [score:3]
First, we detected the effect of overexpression miR-190a on androgen signaling in LNCaP cells. [score:3]
In order to determine the expression of miR-190a, AR, YB-1, CDKN1A, and Ki-67 in tumor tissues, we conducted RT-PCR and IHC staining on tumor samples. [score:3]
As shown in Fig. 7d, patients with high PSA levels (>20) had a lower miR-190a expression, suggesting an inverse correlation between miR-190a and AR in clinical prostate cancer specimens. [score:3]
To investigate the role of miR-190a in inhibition of prostate cancer growth in vivo, we established C4-2 cells stably expressing miR-190a or miR-SC. [score:3]
Through in situ hybridization using digoxigenin-labeled locked nucleic acid (LNA)-miRNA probes we first examined miR-190a expression in 36 cases of human prostate cancer and 8 adjacent normal tissue samples obtained from tissue array. [score:3]
To explore this possibility, we first overexpressed miR-190a with simultaneous depletion of YB-1 in LNCaP cells. [score:3]
The miR-190a targeting sites in 3′UTRs of human YB-1 are shown. [score:3]
Our results, for the first time, provide compelling evidence further rationalizing the targeting strategy to disengage the functional interaction between miR-190a and AR signaling in clinical practice to treat prostate cancer. [score:3]
Overexpression of miR-190a significantly reduced both the tumor size and the tumor weight (Fig. 6a–c). [score:3]
Overexpression of miR-190a contributes to prostate cancer growth in CSPC and CRPC. [score:3]
The miR-190a expression was used to assign the samples to high (upper 50th percentile) or low (lower 50th percentile) groups. [score:3]
The Kaplan-Meier analysis was conducted to evaluate the difference in disease-free survival associated with high versus low expression levels of miR-190a. [score:3]
In vivo tumor implantation C4-2 cells stably expressing miR-190a and miR-SCR were injected subcutaneously into 4-6-week-old castrated mal nude mice purchased from Beijing HFK Bio-Technology. [score:3]
Taken together, these data indicate that YB-1 is required for miR-190a -mediated suppression of AR protein levels and activity (Fig. 4g). [score:3]
LNCaP cells with miR-190a overexpression were treated with DHT for 16 hrs. [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]
To further investigate whether miR-190a -mediated inhibition of cell proliferation is dependent on AR, we overexpressed miR-190a in LNCaP cells followed by DHT treatment. [score:3]
miR-190a expression by qRT-PCR. [score:3]
How to cite this article: Xu, S. et al. The inhibitory effects of AR/miR-190a/YB-1 negative feedback loop on prostate cancer and underlying mechanism. [score:3]
Bioinformatics analysis and 3′-UTR luciferase reporter assays demonstrated YB-1 was a direct target of miR-190a. [score:3]
C4-2 cells stably expressing miR-190a and miR-SCR were injected subcutaneously into 4-6-week-old castrated mal nude mice purchased from Beijing HFK Bio-Technology. [score:3]
MiR-190a expression is repressed by AR upon androgen treatment. [score:2]
MiR-190a inhibits prostate tumor growth in vivo. [score:2]
In order to determine whether miR-190a regulates AR signaling, we established stable cell lines (LNCaP, C4-2, and 22Rv1) through lentiviral transduction. [score:2]
miR-190a expression in AR -positive cell lines was detected at lower levels (LNCaP, C4-2, LAPC4, 22Rv1) when compared to AR -negative cell lines (RWPE1, PC3, DU145) (Supplemental Fig. 1a,b). [score:2]
In order to validate bioinformatics analysis, which indicated that only YB-1 was a potential target of miR-190a (Fig. 4a), we performed luciferase assays using reporters containing wild-type YB-1 3′-UTR and mutant defective for miR-190a binding (Fig. 4a). [score:2]
Taqman RT-qPCR was performed to detect mature miRNA expression using Taqman miRNA reverse transcription kit, has-miR-190a (AB Assay ID: 000489) and RNU6B (U6, AB Assay ID: 001093) according to the manufacturer’s protocol (Applied Biosystems) 35. [score:1]
We next analyzed the relationship between miR-190a and PSA. [score:1]
Furthermore, we identified the half ARE site in the promoter region of the miR-190a gene. [score:1]
A significant negative correlation between miR-190a and AR in clinical prostate cancer specimens. [score:1]
As shown in Fig. 1b, qRT-PCR analysis revealed that miR-190a levels were decreased upon androgen treatment in LNCaP cells. [score:1]
As shown in Fig. 1i, AR was detected in the P2 (−395 to −229) and P3 (−584 to −411) regions of miR-190a promoter with an increased association to the promoter in the presence of DHT. [score:1]
This result showed androgen/AR -dependent repression of miR-190a transcription functions through the promoter of miR-190a gene. [score:1]
The promoter region of miR-190a was cloned upstream of luciferase coding sequence and two separate clones (A-luc: −9 to −1053 containing the ARE; B-luc: −1121 to −2013 lacking ARE) were obtained. [score:1]
PSA-Luc and ARE4-Luc reporter genes were described 31. miRNA luciferase reporters containing the 3′-UTR of YB-1 with miR-190a were provided by Dr. [score:1]
Next, we analyzed the levels of miR-190a in several most commonly used prostate cell lines. [score:1]
We analyzed the region between 2,000-bp and 1-bp upstream of miR-190a promoter and identified two putative half site for ARE (Fig. 1e). [score:1]
miR-190a and AR were inversely correlated in human prostate cancer (r = −0.3935, p = 0.012, n = 40) (Fig. 7f), further supporting the results obtained from in situ hybridization. [score:1]
Taken together, these data suggest that AR -dependent signaling is involved in miR-190a repression of cell growth. [score:1]
miR-190a and AR inverse correlation in human prostate cancers (r = −0.3935, p = 0.012). [score:1]
In summary, we identified a biochemical and functional link between miR-190a, YB-1 and AR signaling in prostate cancer. [score:1]
Oligonucleotide sequences were: LNA-miR-190a: 5′-UGAUAUGUUUGAUAUAUUAGGU-3′. [score:1]
Our study reveals a novel mechanism by which miR-190a influences AR signaling. [score:1]
DHT repressed activity of miR-190a gene reporters ((−9 to −1053) in the presence of AR. [score:1]
Human prostate cancer cells LNCaP, C4-2, PC-3, DU-145, 22Rv1 and benign prostate epithelial cell line, RWPE-1, were purchased from the American Type Culture Collection (ATCC) 24. pLe-miR-SCR lentivirus vector and pLe-miR-190a were purchased from Open Biosystems, AL, USA. [score:1]
To determine the functional significance of miR-190a in regulating the growth of AR -positive prostate cancer cells, we conducted MTT and colony formation assays. [score:1]
LNCaP, C4-2 and 22Rv1 cells infected with pLe-miR-SCR or pLe-miR-190a following by the selection with puromycin. [score:1]
These results suggest a functional interaction between miR-190a and AR during prostate cancer progression. [score:1]
Little is known about whether androgen/AR signaling affects miR-190a signaling in the physiological and pathological conditions of prostate. [score:1]
[1 to 20 of 79 sentences]
[+] 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]
[1 to 20 of 45 sentences]
[+] score: 29
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]
Of its four isoforms (a, a-3p, a-5p, b), miR-190a has been experimentally validated and located on the plus strand of chromosome 15, within the second intron of the gene TALIN2 (TLN2). [score:1]
[1 to 20 of 9 sentences]
[+] 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]
[1 to 20 of 3 sentences]
[+] 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]
[1 to 20 of 14 sentences]
[+] 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]
[1 to 20 of 5 sentences]
[+] 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]
[1 to 20 of 4 sentences]
[+] score: 11
Surprisingly, we found that 2 up-regulated miRNAs, hsa-miR-584-5p and miR-190a, were co-regulated by DELTA 133 p53 mRNA, which is known to be involved in tumourigenesis. [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]
The miRNAs are namely hsa-miR-516a-3p, hsa-miR-125b, hsa-miR-190a, hsa-miR-106a and hsa-miR-584-5p. [score:1]
[1 to 20 of 3 sentences]
[+] 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]
[1 to 20 of 1 sentences]
[+] score: 8
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-580, hsa-mir-588, hsa-mir-190b
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: 6
Other miRNAs from this paper: mmu-mir-190a, mmu-mir-190b, hsa-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
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]
Phylogenetic tree of miR-190/171 family and sequence alignments of hsa-miR-190a/b and sly-MIR171a. [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]
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]
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]
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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]
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[+] 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-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
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: 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
Increased expression of miR-190 may cause decreased IGF-1 in HCC development. [score:4]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-190a, mmu-mir-190b, hsa-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
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 total, there were 12 miRNAs with significantly higher expression (q<0.1) compared to mean of every other tissue, and no such snoRNAs, with mir-126-3p, mir-340-3p, mir-190a, and mir-335-3p showing the strongest specificity signal (Figure 2B). [score:2]
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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-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, hsa-mir-190b, 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: 1
Other miRNAs from this paper: hsa-mir-190b
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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[+] score: 1
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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[+] score: 1
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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[+] score: 1
These include miR-145, let-7d, miR-335, miR-98, miR-181a, miR-200a, miR-373*, miR-575, miR-335, miR-96-5p, miR-190a, miR-29c-3p, and miR-219-5p [7, 8, 13, 14]. [score:1]
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[+] score: 1
An at least twofold greater induction in C57BL6/J mice was detected in eight miRNAs (miR-190a-3p, miR-449a-5p, miR-449a-3p, miR-449c-5p, miR-3096a-5p, miR-3096b-5p, miR-3096b-3p, and miR-669c-5p). [score:1]
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[+] score: 1
0126087.g002 Fig 2(a) Comparison of qRT-PCR data with NGS data for the six novel miRNA candidates {shown in (Fig 1b)} and four known miRNAs (hsa-miR-99b-3p, hsa-miR-190a, hsa-miR-3614-5p and hsa-miR-99a-3p). [score:1]
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[+] score: 1
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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[+] 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-22, hsa-mir-29a, hsa-mir-30a, 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-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
miRNA Fold Change P-value mmu-miR-337-5p −5.2 0.0149 mmu-miR-3544-3p −5.1 0.0147 mmu-miR-540-5p −4.9 0.0200mmu-miR-337-3p [a] −3.0 0.0324mmu-miR-3544-5p [a] −3.0 0.0308 mmu-miR-434-3p −2.1 0.0001 mmu-miR-3071-5p −2.0 0.0004mmu-miR-136-3p [a] −2.0 0.0004mmu-miR-3071-3p [a] −1.6 0.0000 mmu-miR-136-5p −1.6 0.0000 mmu-miR-143-5p −1.2 0.0004 mmu-miR-190a-5p −1.0 0.0139 mmu-miR-872-3p −0.9 0.0152 mmu-miR-193a-3p −0.9 0.0164 mmu-miR-144-3p −0.8 0.0298 mmu-miR-127-3p −0.7 0. 0002mmu-miR-434-5p [a] −0.6 0.0082 mmu-miR-148a-3p −0.6 0.0130 mmu-miR-411-5p −0.6 0.0091 a miRNA* (passenger) strand processed from opposite arm of the mature miRNA. [score:1]
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[+] score: 1
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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[+] score: 1
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-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, hsa-mir-190b, 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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[+] 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-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-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-190b, 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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