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62 publications mentioning hsa-mir-301b

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-301b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 156
Other miRNAs from this paper: hsa-mir-130a, hsa-mir-301a, hsa-mir-130b
As described above, the deregulation of miR-130b and miR-301b has been observed in several PrCa miRNA profiling studies, with the majority of them showing an upregulation of the cluster expression in malignancy as depicted in Table  1. Several studies evidenced a positive association of miR-130b/301b cluster expression and clinicopathological parameters, comprising cancer disease diagnosis [22, 38, 40– 42], presence of local and distant metastasis [59], disease stage [59], Gleason Score [59], pre-operatory PSA [54], disease recurrence [44– 48, 55] and patient overall survival [38, 59]. [score:15]
It was proposed that miR-301b expression is induced in vitro by hypoxia in PrCa cell lines (DU145, PC-3, LNCaP) causing an increase of autophagy, leading to the loss of radio-sensitivity [51]; the same report proposed tumor suppressive hydrolase NDRG2 as a direct target of miR-301b. [score:8]
DNMT1 was listed by TarBase but not included in this list since the referenced article demonstrates the absence of effect of miR-301b on DNMT1 [b]Direct target genes with experimental validation in PrCa [c]Direct Targets predicted in PrCa. [score:7]
We included the 7 direct targets reported in PrCa (MMP2, DEDD2, NDRG2, AR, LMNB1, PARVA, SLC8A1) and 16 direct targets empirically validated in other cancers compiled in TarBase (RUNX3, TP53INP1, PPARG, CSF1, UVRAG, ZEB1, DICER1, STAT3, PDGFRA, ZBTB4, PTEN, SMAD4, ITGB1, CCNA2, PPARGC1A, FMR1 for miR-130b and TP63 and DNMT1 for miR-301b) [61] (Table  2). [score:7]
The expression profile of miR-130b and miR-301b, their correlation with candidate TSG targets, as well as their association with PrCa aggressiveness in the TCGA-PRAD support an oncogenic function for these miRNAs for the disease. [score:7]
For each target gene the role in PrCa, the literature reference (PMID) and the correlation r and p value are shownQualifiers in column 1 indicate: [a]miR-301b direct target with strong experimental evidence assigned by TarBase. [score:6]
Table 2 Association between the expression of miR-130b/301b and putative direct target genes in TCGA-PRAD Gene PMID Role in PrCa miR-130b miR-301b r p value r p value PPARGC1A 23868745 TSG? [score:6]
The correlation between the expression of validated direct targets of miR-130b and miR-301b supports their oncogenic function in PrCa. [score:6]
Secondly, Ramalho-Carvalho et al. found an expression profile and a function consistent with a tumor suppressor role of miR-130b and miR-301b in PrCa, showing their ability to reduce cell viability, induce DNA damage, apoptosis and cell senescence [29]. [score:5]
Indeed, a tumor suppressor function has been proposed for miR-130b [29, 52] and miR-301b [29], which were shown to inhibit PrCa invasion, homing or cell cycle progression. [score:5]
b Expression of miR-301b in normal and tumor (normal = 22, Tumor = 273) prostate tissues obtained from small RNA-seq data of TCGA-PRAD cohort The molecular basis for the increment of miR-130b and miR-301b expression in tumors is currently unknown. [score:5]
Correlation between miR-301b and target mRNAs expression in TCGA-PRAD. [score:5]
We confirmed an upregulation of both miR-130b and miR-301b in tumor vs normal tissue in TCGA-PRAD specimens. [score:4]
a- miR-301b direct targets with strong experimental evidence assigned by TarBase. [score:4]
Meanwhile, miR-301b shows a tendency to be upregulated in unmatched tumor vs normal tissue (1.20-fold, p 0.0852); its low abundance may explain the lack of significance of the change (Fig.   2b). [score:4]
The examination of nucleotide and structural variation of the region in the TCGA-PRAD (492 samples) using cBioPortal [56] only identifies 5 copy number variants for miR-301b (1 amplification and 4 deep deletions), suggesting that DNA sequence changes are unlikely to be responsible for the upregulation of this cluster observed in tumors. [score:4]
On the contrary, 5 studies found that either miR-301b, miR-130b or both are downregulated in PrCa, including malignant tissue [29, 52], high Gleason Score tumors [53], high pre-operatory PSA levels [54] and recurrent patients [53, 55]. [score:4]
These candidates are expected to correlate negatively with the expression of miR-130b or miR-301b in PrCa if the oncogenic hypothesis holds true in the clinical samples. [score:3]
Meanwhile, we were unable to find any significant association between miR-301b tissue abundance in PrCa and the clinical presentation of the disease. [score:3]
As an example, only 54% (294) of the TCGA-PRAD samples detect expression value of miR-301b (Fig.   1c). [score:3]
Chr chromosome miRNA microRNA miR-130b hsa-miR-130b-3p miR-301b hsa-miR-301b-3p OG oncogene PRAD prostate adenocarcinoma PrCa prostate cancer RPM reads per million TCGA The Cancer Genome Atlas TSG tumor suppressor gene Study conception MAD, Study design MAD, Acquisition of the clinical data RSF, Analysis of the data RSF, CM, COR, Interpretation of the data RSF, CM, COR, JRSS, MAD, Drafting of the manuscript MAD, Critical Revision RSF, CM, COR, BG, JRSS, MAD. [score:3]
c Co -expression of miR-130b and miR-301b in prostate clinical samples of TCGA-PRAD, including normal and tumor tissue. [score:3]
Yet, a small proportion of studies have reported a negative association between miR-130b/301b expression and tumor status [29, 52] (miR-130b and miR-301b), preoperatory PSA [54] (miR-130b) and biochemical recurrence (miR-130b in serum in [53] and miR-301b in tissue [55]). [score:3]
The miR-130b and miR-301b are expressed in PrCa and their abundance is positively associated with the DNA methylation of their locus. [score:3]
n = 294 (samples that report expression data for miR-301b). [score:3]
We thoroughly revised the PrCa literature and found 25 independent articles in which a differential expression of miR-130b or miR-301b is recognized. [score:3]
Fig.  2Expression of miR-130b and miR-301b in normal and tumor prostate tissue. [score:3]
The failure of miR-301b to associate with clinical variables may be due to its reduced expression in prostatic tissue relative to miR-130b. [score:3]
The expression of miR-130b and miR-301b associates with negative PrCa patient clinical outcome. [score:3]
We analyzed the putative association between the expression of miR-130b and miR-301b and the clinical data, including preoperative PSA, Gleason Score, number of positive lymph nodes, pathological N-stage, pathological T-stage, residual tumor, primary therapy outcome success and biochemical recurrence. [score:3]
The expression of miR-130b and miR-301b increases in PrCa neoplastic tissue and metastasis. [score:3]
The precursor RNAs hsa-mir-130b and hsa-mir-301b are processed preferentially from the 3′ arm of the hairpin to generate mature miRNAs hsa-miR-130b-3p and hsa-miR-301b-3p (hereafter referred as miR-130b and miR-301b, respectively). [score:1]
The stem-loop precursors of miR-130b and miR-301b are coded 327 bp apart, where mir-301b is in the first intron of the transcript (chr22:22007270-22007347 of GRCh37/hg19 or chr22:21652981-21653058 of GRCh38/hg38) and mir-130b spans from the first intron to the beginning of exon 2 (chr22:22007593-22007674 of GRCh37/hg19 or chr22:21653304-21653385 of GRCh38/hg38) (see Fig.   1b and Additional file 1: Figure S1 for a detailed view of the region). [score:1]
Correlation between the levels of miR-301b (x axis) and miR-130b (y axis) of the TCGA-PRAD cohort. [score:1]
Fig.  3Pattern of DNA methylation of the miR-130b/miR-301b locus in prostate tissue of TCGA-PRAD. [score:1]
The level of increase in miRNA abundance in malignant samples is 1.2–8.6 folds for miR-130b (p 0.05 to < 0.0001) and 1.5–2.2 folds for miR-301b (p 0.025 to < 0.0066). [score:1]
In the human genome, it is composed by four miRNA precursor genes: mir-301a (at chr17), mir-130a (at chr11), mir-130b and mir-301b (at chr22). [score:1]
Meanwhile, oncogenic MMP2, proposed to be repressed by the cluster in a study in PrCa, shows a weak negative correlation with the miRNAs (r − 0.11 p = 0.01 for miR-130b and r − 0.13 p = 0.03 for miR-301b). [score:1]
Of note, miR-301b is about ten time less abundant than miR-130b in prostatic tissue (Fig.   1c), and this probably explains why the former is less reported in the literature. [score:1]
Pattern of DNA methylation of the miR-130b/miR-301b locus in prostate datasets. [score:1]
Pattern of DNA methylation of the miR-130b/miR-301b locus in prostate cell lines. [score:1]
Meanwhile, an oncogenic role has been proposed for miR-130b [38, 44, 62] and miR-301b [63] in PrCa, which were revealed to promote cell proliferation, viability, migration, invasion or tumor initiating properties. [score:1]
hsa-miR-301b hsa-miR-130b TCGA miRNA Prostate Cancer DNA Methylation Transcriptome Microarray Clinical outcome Worldwide, prostate cancer (PrCa) is the second most frequently diagnosed cancer and the sixth major cause of cancer-related deaths in men. [score:1]
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2
[+] score: 40
Two of these miRNA clusters (miR-143-145 at 5q32 and miR-497-195 at 17p13.1) were markedly down-regulated in triple -negative breast cancer, while the other five miRNA clusters (miR-17-92 at 13q31.3, miR-183-182 at 7q32.2, miR-200-429 at 1p36.33, miR-301b-130b at 22q11.21, and miR-532-502 at Xp11.23) were up-regulated in triple -negative breast cancer. [score:7]
Furthermore, our work extends the potential target network of miRNAs by showing that the cyclin G2 gene (CCNG2) is a direct target of miR-130b-5p from the miR-301b-130b cluster. [score:6]
Quantitative RT-PCR data confirmed that miR-301b-5p, miR-130b-5p, and miR-130b-3p were all up-regulated in 19 triple -negative breast cancer samples (Figure  3B-D, respectively). [score:4]
All three miRNAs in the miR-301b-130b cluster were markedly up-regulated in triple -negative breast cancer. [score:4]
Moreover, we extended the current knowledge of microRNA regulatory network by showing that miR-130b-5p in the miR-301b-130b cluster directly silences CCNG2 in triple -negative breast cancer. [score:3]
Figure 3 RT-PCR validations of the differentially expressed miRNAs in the miR-301b-130b cluster and the miR-497-195 cluster. [score:3]
Moreover, miR-130b-5p from the miR-301b-130b cluster was shown to directly repress the cyclin G2 (CCNG2) gene, a crucial cell cycle regulator, in triple -negative breast cancer cells. [score:3]
These overexpressed miRNAs include four miRNAs (p <0.05; fold change 1.9-3.0) in the miR-17-92 cluster, five miRNAs (p <0.05; fold change 2.5-3.8) in the miR-183-182 cluster, four miRNAs (p <0.05; fold change 1.7-3.1) in the miR-200b-429 cluster, three miRNAs (p <0.05; fold change 2.2-3.6) in the miR-301b-130b cluster, and eight miRNAs (p <0.05; fold change 2.0-2.6) in the miR-532-502 cluster. [score:3]
Relative expression levels of (B) miR-301b-5p, (C) miR-130b-5p, and (D) miR-130b-3p in triple -negative breast cancer tissues (n = 19) and adjacent normal tissues (n = 4) are shown. [score:3]
To confirm the results obtained from the sequencing data, quantitative RT-PCR validations were carried out to examine the expression levels of the miRNAs residing in the miR-532-502 cluster, the miR-301b-130b cluster, and the miR-497-195 cluster in 19 triple -negative breast cancers and 4 adjacent normal tissues using the comparative C [T] method [13]. [score:3]
Figure  3A shows the specific miRNA forms at each locus in the miR-301b-130b cluster. [score:1]
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3
[+] score: 37
A total of seven miRNAs deregulated in R. rickettsii-infected endothelial cells were thus further confirmed in this study, of which four (miR-129-5p, miR-200a-3p, miR-200b-3p, and miR-595) were up-regulated and another three (miR-301b-3p, miR-548a-3p, and miR-377-3p) were down-regulated. [score:8]
We also quantified the expression of mRNAs for SOD1 and SOD2 as targets of miR-377-3p, and miR-301b-3p, both of which are subjected to negative regulation in R. rickettsii-infected host endothelial cells. [score:6]
Intriguingly, SOD1 and SOD2 are validated targets of miR-377-3p and miR-377-3p/miR-301b-3p, respectively, and both of these miRNAs are down-regulated in our system, suggesting the to-be-tested hypothesis for potential correlation between changes in the transcription of inducible SOD isoforms and selective host miRNAs due to rickettsial infection. [score:6]
Similarly, q-RT-PCR based analysis of the expression patterns of miR-301b-3p, miR-548a-3p, and miR-377-3p, which were determined to display diminished expression by microarray -based measurements (Figure 2A), also demonstrated consistent, statistically significant down-regulation of all three miRNAs (Figure 2B–D). [score:6]
Again, q-RT-PCR based quantitation on day 3 post-infection (Figure 3) revealed about 7.0 ± 1.9-fold higher expression of miR-129-5p (A) and 4.7 ± 0.9-fold up-regulation of miR-200a-3p (B) in the lungs of infected mice when compared to the uninfected controls and a decrease of about 53 ± 5% in the levels of miR-301b-3p (C) and 51 ± 10% in miR-377-3p (D), respectively. [score:5]
Again, our results indicate significant induction of SOD1 (E) and SOD2 (F) mRNA post-infection in concordance with the decrease in miR-377-3p and miR-301b-3p expression (Figure 2). [score:3]
As an important corollary to these in vitro findings, we further analyzed the expression status of miR-129-5p, miR-200-3p, miR-301b-3p, and miR-377-3p in the lungs of mice infected with R. conorii, another spotted fever group pathogen phylogenetically and antigenically similar to R. rickettsii. [score:3]
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[+] score: 22
A significant number of genes associated with metastasis were overexpressed in tumors classified into the serum miRNA cluster 1. (A) Box plots representing microarray expression results for miR-141, miR-200b, miR-193b and miR-301 from two different studies performed in lung primary tumors. [score:5]
A supervised diagnostic miRNA signature composed of 4 miRNAs (miR-141, miR-200b, miR-193b and miR-301) which were up-regulated in NSCLC tumors and serum was selected to validate its diagnostic value in an independent cohort of age and sex-matched serum samples. [score:4]
We identified 4 miRNAs that fulfilled these criteria: miR-141, miR-200b, miR-193b and miR-301, since they were significantly overexpressed in lung AC and/or SCC versus normal lung samples (Fig. 3A) as well as in the serum of NSCLC patients versus NC (Fig. 3B). [score:3]
Validation results showed that all 4 miRNAs were significantly overexpressed in the NSCLC sera (p < 0.001) and the log [2] fold-change for miR-141, miR-200b, miR-193b and miR-301 were 2.67, 2.98, 2.52 and 2.01 respectively. [score:3]
All four miRNAs were significantly overexpressed (p < 0.001) in lung tumors, except miR-301 that was not significantly higher in lung SCC. [score:3]
MiR-301 was found overexpressed among vesicle-related miRNAs from plasma in NSCLC 20, but it has not been previously reported as a serum -based marker for cancer diagnosis. [score:3]
To validate these findings, we measured by RT-PCR the expression level of miR-141, miR-200b, miR-193b and miR-301 in the serum of an independent cohort of 84 NSCLC and 23 age and sex-matched NC subjects. [score:1]
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5
[+] score: 21
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-21, hsa-mir-23a, hsa-mir-27a, hsa-mir-29a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-301a, hsa-mir-378a, hsa-mir-381, hsa-mir-340, hsa-mir-146b, hsa-mir-181d, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-590, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-378d-2, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-378c, hsa-mir-23c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, 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-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Namely, HHV-6A specifically induced an early up-regulation of miR-590 (1 d. p. i. ), miR-15a and miR-21 (3 d. p. i. ), a sustained up-regulation of miR-29b, miR-101 (3 and 6 d. p. i. ), miR-301a and miR-548e (1 and 6 d. p. i. ) and a late up-regulation of miR-340 and miR-381 (6 d. p. i. ) By contrast, HHV-6B infection specifically up-modulated the expression of miR-301b (2 and 3 d. p. i. ) and miR-548e (1 and 3 d. p. i. ), whereas it down-regulated miR-590 (2 and 3 d. p. i. ) and miR-15a (6 d. p. i. ). [score:15]
Interestingly, miR-301 was also up-regulated in T cells in the central nervous system of animals with experimental autoimmune encephalomyelitis (Mycko et al., 2012), an animal mo del for the process of autoimmune demyelination occurring during multiple sclerosis, a disease with a possible association with HHV-6 infection (Leibovitch and Jacobson, 2014). [score:6]
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6
[+] score: 20
miR-301b promoted cell migration and invasion in bladder cancer through downregulating the expression of PTEN, which suggests that miR-301b-3p might target the 3′-UTR of PTEN and regulate the aggregation of tau [44]. [score:9]
MiR-342-5p, miR-3058-3p, let-7f-5p, miR-1961, miR-301b-3p, miR-98-5p, miR-1251-5p, miR-215-5p, miR-881-5p, miR-135a-2-3p, and miR-33-3p may regulate the expression of insulin-like growth factor 1 (IGF1) or insulin-like growth factor 2 (IGF2), two molecules that could rescue behavior and memory deficits via lowering A β levels [28, 29]. [score:4]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
Several miRNAs derived from our microarray analysis targeted PTEN, such as miR-376c-3p, miR-342-3p, let-7f-5p, miR-10a-5p, miR-301b-3p, miR-98-5p, miR-1251-5p, and miR-34a-5p. [score:3]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
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7
[+] score: 19
Interestingly, 7 of the 12 miRNAs that were up-regulated in the presence of IFN-α (miR-30b,miR-30c, miR-130a, miR-192, miR-301, miR-324-5p and miR-565) were also down-regulated in HCV -infected Huh7.5 cells. [score:7]
Seven miRNAs (miR-30b, miR-30c, miR-130a, miR-192, miR-301, miR-324-5p, and miR-565) were down-regulated in HCV-infected Huh7.5 cells (p<0.05) and subsequently up-regulated following interferon-α treatment (p<0.01). [score:7]
The GOMir tool JTarget, using five major miRNA-mRNA prediction databases, identified a list of mRNA targets for miR-30, miR-130a, miR-192, miR-301 and miR-324-5p [21]. [score:5]
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8
[+] score: 15
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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Such a situation occurred for miR-26b, miR-30, and miR-374 downregulation, and for miR-34, miR-301, and miR-352 upregulation [121]. [score:7]
Of these miRNAs, 12 were upregulated (miR-34b, miR-138, miR-297a, miR-301, miR-449, miR-466, miR-493, miR-579, miR-582, miR. [score:4]
Three dysregulated miRNAs (miR-301, miR-369, and miR-669k) overlapped in the lungs of adenoma-bearing mice and of microadenoma-bearing mice. [score:2]
These miRNAs were miR-301, miR-369, and miR-669k, whose main functions are to regulate cell proliferation, autophagy, and aerobic glycolysis, which are mechanisms involved in the initial stage of the functional transformation of cells into their neoplastic counterpart. [score:2]
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9
[+] score: 15
Calin et al. reported that one cluster of FRAs at chromosome 17q23 contains three HPV16 integration events and four miRNA genes (miR-21, miR-301, miR-142s, and miR-142as); they conclude that these miRNAs are possible targets of such viral integration that may lead to deregulation of miRNAs expression [8]. [score:6]
So, overexpression of miR-301b could potentially increase RAS activation and promote CC via the downregulation of RASAL1 (Figure 1). [score:6]
miR-301b is overexpressed in colon cancer tissue [66] and CC (Table 1) [43]. [score:3]
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10
[+] score: 14
Other miRNAs from this paper: hsa-mir-21, hsa-mir-301a
The OS of BC patients with high miR-301a expression was significantly higher than that of those patients with low miR-301 expression. [score:5]
Based on a study by Shi et al., a novel oncogenic role for miR-301 through the regulation of key signalling pathways involving PTEN, FOXF2, and Col2A1 was identified, and miR-301 overexpression was associated with an increased risk of distant relapse and resistance to tamoxifen [26]. [score:4]
More importantly, both the univariate and multivariate survival analyses demonstrated that high miR-301a expression was correlated with shorter DFS and OS in BC patients, which was also consistent with the prognostic significance of miR-301 in other human malignancies, such as gastric cancer [17] and melanoma [18]. [score:3]
Here, the focus is on miR-301. [score:1]
Intronic miR-301a, which is one of two mature forms of miR-301 (miR-301a and miR-301b), and its host gene, SKA2 (spindle and kinetochore -associated protein 2), are located on chromosome 17q22–23 in the human genome [25]. [score:1]
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11
[+] score: 14
An unpaired t-test revealed 7 miRs with significant differences in expression: miR-146a-5p, miR-301b and miR-138 displayed higher expression in epiphyseal cells while miR-143, miR-146a, miR-34a and miR-145 displayed higher expression levels in diaphyseal cells (A). [score:7]
Only 7 miRs were identified with a statistically significant difference in expression between epiphyseal and diaphyseal cells (Figure 4A), namely: miR-146b-5p, miR-301b and miR-138 (higher expression in epiphyseal cells) and miR-143, miR-145, miR-146a and miR-34a (increased expression in diaphyseal cells). [score:7]
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12
[+] score: 10
Other miRNAs from this paper: mmu-mir-301a, hsa-mir-301a, mmu-mir-301b
It is possible, however, that living cells have evolved a buffering mechanism whereby the loss of Oct4 down-regulates mir-301, which in turn up-regulates its paralogs Pou4f1, Pou3f2 or Pou4f2, which compensate for the function of Oct4. [score:7]
Previous experiments have shown that Oct4 can affect transcription of the microRNA mir-301 [39], which in turn targets the Oct4 paralogs Pou4f1, Pou3f2 and Pou4f2. [score:3]
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13
[+] score: 9
With the exception of miR-301, all of these putative REST target miRNAs were found to be expressed in both NT2-N and PHN, and many of them were differentially expressed between neurons and astrocytes suggesting that they may be regulators of neuronal development and function (Fig. 8). [score:9]
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14
[+] score: 9
Considering these findings, we speculate that controversial effects may not occur among different cell types, and we anticipate a consistent effect of miRNA-301a regulation of ASK1 expression and activation on hASCs [miR-301] transplanted into infarcted hearts. [score:4]
Figure 5C shows that transplanted hASCs [miR-301] had greater survivorship rates than transplanted hASCs at injected sites, with less cell death observed in hASCs [miR-301] injected heart tissue (Figure 5D). [score:1]
The fibrosis area was significantly reduced by hASCs [miR-301] injection in ischemic hearts (Figure 5B). [score:1]
Effect of hASC [miR-301] on Ischemic Myocardium. [score:1]
To determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
Effect of hASC [miR-301] on Ischemic MyocardiumTo determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
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15
[+] score: 9
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-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, 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-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, 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-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, 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-1-2, hsa-mir-15b, hsa-mir-23b, 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-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, 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-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, 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-301a, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
This report indicated that bmp3, hsp60, and msxb genes had role in regeneration and were predicted targets of up- or downregulated miR-200b, miR-2/miR-338, and miR-301, respectively. [score:6]
Ramachandra et al. (2008) Oocyte and early embryo miR-34 Zebrafish Knockdown, microarray, qRT–PCR Nervous system development Soni et al. (2013) Oocyte miR-15, miR-29, miR-92, miR-101, miR-126, miR-181-3p, miR-196, miR-202-5p, miR-202-3p, miR-221, miR-301, miR-338, and miR-2184 Rainbow trout Microarray ? [score:3]
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16
[+] score: 8
In the current study, the miRNA expression changes produced following the stimulation of CD3 [+] T cells with anti-CD3 antibodies suggests that Th17/Treg polarization was associated with the induction of miR-146a, miR-21, and miR-155 expression; that together with miR-301 up-regulation, this process would result in a Treg bias. [score:8]
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17
[+] score: 8
HHV-6A infection, but not -6B or −7 infections, induced a decrease in miR-155_2 expression and an increase in miR-1238 expression in thyrocytes, as well as an increase in the expression levels of several autoimmunity -associated miRNAs in T lymphocytes, including miR-16_1, miR34a, miR-130a, miR-143_1, miR-202, miR-301b, miR-302c, miR-449b, miR-451_1, and miR-1238_2. [score:7]
In fact, HHV-6A infection (but not HHV-6B or HHV-7 infection) induced a remarkable increase in several autoimmunity-related miRNAs, namely: miR-16, miR-34a, miR-130a, miR-202, miR-301b, miR-302c, and miR-449b. [score:1]
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18
[+] score: 8
Importantly, this regulatory loop involves both transcriptional and post-transcriptional regulatory mechanisms, as OCT4 not only binds the SRSF2 promoter, but it also negatively regulates the expression of miRNAs targeting its 3′UTR, such as miR-301b and miR-130b [208]. [score:8]
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[+] score: 8
In particular, CUL3, over expressed in kidney and prostate cancers, is a target of several dysregulated MIRs: MIR22, MIR23A, MIR23B, MIR218-1, MIR218-2, and MIR301, which are down regulated in kidney cancers, and of MIR22, MIR23A, MIR181A, and MIR181C, which are down regulated in prostate cancers (Table 5). [score:8]
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[+] score: 8
In the second group, there were six miRNAs with an expression level that was four times lower in BCSCs than in MCF-7 cells: miR-200a, miR-301, miR-188, miR-21, miR-181d and miR-29b. [score:3]
Moreover, miR-301, miR-296, miR-21 and miR-373* have been reported to be expressed in human embryonic stem cells and other stem cells, indicating that these miRNAs may play a constitutive role in maintaining the biological characteristics of stem cells [40, 41]. [score:1]
We performed real-time RT-PCR for 10 miRNAs: miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
The analysed miRNAs included miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
Parts of the amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown (B). [score:1]
Part of amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown in Figure 3B. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-155, bta-mir-155, bta-mir-301b
However, a number of other nearby genes also have merit including (1) immunoglobulin lambda-like polypeptide 1 precursor (IGLL-1) which has been observed to have increased expression in bovine udder tissue in response to Streptococcus uberis challenge (Swanson et al., 2009), (2) Synaptosomal -associated protein 29 (SNAP29) whose increased expression has been linked to enhanced internalization and killing of E. coli by mast cells (Wesolowski et al., 2012), (3) Stromal cell-derived factor 2-like protein 1 (SDF2L1) which is involved in the processing of a wide range of defensins and (4) mir301b, a microRNA which has been shown to be significantly down-regulated in response to lipopolysaccharide (LPS) (Zheng et al., 2012). [score:8]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-301a, hsa-mir-630
In prostate cancer, luteolin exerts anticancer effects through various mechanisms such as suppression of androgen receptor expression and vascular endothelial growth factor receptor 2 (VEGFR-2) mediated angiogenesis at > 10 μM, and induction of cytotoxicity, apoptosis and cell cycle arrest via regulation of IGF-1/Akt pathway, Akt-Mdm2 pathway, epidermal growth factor signaling pathway and expression levels of miR-630 and miR-301 at > 10 μM [26– 30]. [score:8]
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[+] score: 8
It was demonstrated that LTL could inhibit the proliferation of and induce apoptosis in prostate cancer cells by downregulating the expression of miR-301 [22]. [score:8]
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24
[+] score: 7
We obtained similar results showing the up-regulation of genes (GATA2, SERPINE1, myosin VA, or ubiquitin specific peptidase 33) associated with endocytosis, vesicle -mediated transport, and signal transduction, whereas their corresponding miRNAs were down-regulated (e. g., mir-32, miR- 92a, miR-200c, miR, or miR-301b). [score:7]
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25
[+] score: 7
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Of the up-regulated miRNAs (in the metastatic library), miR-210 has been reported to be up-regulated in prostate carcinomas relative to BPH samples [23] and miR-301 has been linked to prostate cancer metastasis [37]. [score:7]
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[+] score: 7
And some of these miRNAs, such as miR-26b, miR-106a and miR-301b (targeting Hsc 70), or miR-21, miR-224 and miR-373 (targeting LAMP2A) have been confirmed to target the 3' UTR of either Hsc 70 or LAMP2A [42]. [score:7]
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[+] score: 7
Functional screening by in vitro transfection of miRNA mimics and inhibitorsMiRNA mimics for miR-1237, miR-365b-5p, miR-550a-5p and miR-135a-3p and miRNA inhibitors for miR-301b, miR-503, miR-542-5p and miR-210 were chosen for further functional investigation. [score:3]
We performed GO analysis and KEGG pathway analysis on the differentially expressed miRNAs, and the results are shown in Supplementary Figure 1. Ultimately, fifteen potential miRNAs associated with the proliferation of osteosarcoma were selected for microarray validation by quantitative real-time RT-PCR analysis, including miR-1237, miR-550a-5p, miR-365b-5p, miR-135a-3p, miR-933, miR-762, miR-629-3p, miR-542-5p, miR-503, miR-301b, miR-210, miR-374a-5p, miR-199a-5p, miR-199a-3p and miR-195-5p. [score:3]
MiRNA mimics for miR-1237, miR-365b-5p, miR-550a-5p and miR-135a-3p and miRNA inhibitors for miR-301b, miR-503, miR-542-5p and miR-210 were chosen for further functional investigation. [score:1]
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[+] score: 6
For instance, mir-215 and mir-301 are downregulated in colon cancer, and mir-129 is overexpressed in prostate cancer. [score:6]
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[+] score: 6
Developmental expression profiling of the murine CNS revealed 12 miRNAs (miR-9, miR-17-5p, miR-124a, miR-125a, miR-125b, miR-130a, miR-140, miR-181a, miR-199a, miR-205, miR-214, miR-301) with significantly higher expression at embryonic versus postnatal time points. [score:6]
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[+] score: 6
In addition, three down-regulated miRNAs (miR-206, miR-301 and miR-187) also were predicated to target on AIV genome. [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-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-190b, 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
Three miRNAs, miR-26b, miR-106a and miR301b, have been demonstrated to regulate HSP70 expression, and were also shown to be significantly increased in Parkinson’s disease patients resulting in aberrant α-synuclein aggregation in Lewy bodies [68]. [score:6]
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[+] score: 6
Six genes deregulated between cell lines are targeted by miR-548c, miR-145, miR-301b, and miR-628-5p: Anxa8, Fbn1, Ptx3, Upp1, and Usp33. [score:4]
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: 5
Except for miR-301, no studies have shown direct regulation of FOXF2 by a miRNA. [score:3]
Recently miR-301 was defined as an oncogene and it was reported to mediate proliferation via regulating FOXF2 in breast cancer [36]. [score:2]
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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-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-93, 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-196a-1, hsa-mir-197, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, 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-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, 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-146a, hsa-mir-150, hsa-mir-194-1, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-372, hsa-mir-374a, hsa-mir-375, hsa-mir-328, hsa-mir-133b, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-486-1, hsa-mir-146b, hsa-mir-494, hsa-mir-503, hsa-mir-574, hsa-mir-628, hsa-mir-630, hsa-mir-449b, hsa-mir-449c, hsa-mir-708, hsa-mir-1827, hsa-mir-486-2
MiR-301 is another oncomir upregulated in several types of cancer, including NSCLC, and involved in smad4 repression through the direct binding to 3′ UTR [90- 91]. [score:5]
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[+] score: 5
In breast cancer, global miRNA expression profiling studies have identified significant alterations in a number of oncogenic and tumor-suppressive miRNAs, including miR-221, miR-21, miR-125, and miR-301 [9- 11]. [score:5]
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[+] score: 5
For example, miR-625, miR-103/miR-107, miR-21 and miR-301 have been found to promote CRC to invade and metastasize by stimulating multiple metastasis-promoting genes [27– 30], whereas miR-99, miR-137, miR-132 and miR-128 function as tumor suppressors to inhibit the metastasis of CRC [31– 34]. [score:5]
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37
[+] score: 4
We noticed that there were many miRNAs, such as mir-340-3p, mir-340-5p, mir-1896, mir-546, and mir-301b, whose expression were not significantly affected by Activin A or Wnt3a alone at progression or maturation stages, but regulated by Activin A and Wnt3a co-treatment. [score:4]
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38
[+] score: 4
Cao G, Huang B, Liu Z, Zhang J, Xu H, Xia W, Li J, Li S, Chen L, Ding H, Zhao Q, Fan M, Shen B, Shao N: Intronic miR-301 feedback regulates its host gene, ska2, in A549 cells by targeting MEOX2 to affect ERK/CREB pathways. [score:4]
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39
[+] score: 3
The assay results revealed four highly up-regulated miRNAs (up to 60-fold change) at 24 hpi: miR-29b, miR-155, miR-301a and miR-301b. [score:3]
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40
[+] score: 3
S2 FigScreen-shot of UCSC Genome Browser at (A) miR-17-92a cluster genomic locus (B) miR-301b/130b genomic locus shows the position of mature miRNAs, transcription (RNA-seq data) and H3K27Ac ChIP-seq data (a marker of active promoter) from 9 cell lines (GM12878 (LCL), h1-hESC, HeLa-S3, HepG2, HSMM, HUVEC, K562, NHEK and NHLF), NF-Y ChIP-seq data from 3 cell lines. [score:1]
pri-miRNA n° of CCAAT matrices matrices distance from TSS mir-181a2/181b2 2 ataattggttt -401 agcccaatcag -131 mir-21 3 tatccaatccc 218 atcccaatcat -416 ttaattggttc -102 mir-301b/130b 3 cggccaatgag -55 gagattggagc -254 gggccaatcgg -140 mir-17/18a/20a/19b1/92a1 1 gtgattggcgg -104 10.1371/journal. [score:1]
pri-miRNA n° of CCAAT matrices matrices distance from TSS mir-181a2/181b2 2 ataattggttt -401 agcccaatcag -131 mir-21 3 tatccaatccc 218 atcccaatcat -416 ttaattggttc -102 mir-301b/130b 3 cggccaatgag -55 gagattggagc -254 gggccaatcgg -140 mir-17/18a/20a/19b1/92a1 1 gtgattggcgg -104 10.1371/journal. [score:1]
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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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, 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-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, 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-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
Several research groups demonstrated that miRNA-548d, miRNA-224, miRNA-373, miRNA-198, miRNA-106a, miRNA-26b, and miRNA-301b show altered expression in PD patients (Alvarez-Erviti et al., 2013; Burgos et al., 2014; Cardo et al., 2014). [score:3]
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[+] score: 3
Additionally, the expression level of miR-301, 194, and 122 was lower in the high graded fibrotic liver tissue than in low graded fibrotic liver tissue [18] [19] [20](GEO Series accession number GSE16922). [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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, 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-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mouse and human were: let-7, miR-7, miR-15, miR-101, miR-140, miR-152 (all validated by qPCR, P < 0.05), as well as miR-17, miR-34, miR-135, miR-144, miR-146, miR-301, miR-339, miR-368 (qPCR not performed). [score:3]
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[+] score: 3
Recently, it has been established that the expression of hepatic miRNA (miR-22b, miR-140, miR-210a, mir-301, miR-457b, and let-7d) is increased in fluoxetine (the active ingredient in Prozac®) exposed female zebrafish (Craig et al., 2014). [score:3]
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45
[+] score: 3
Increasing evidence has ascertained that a large number of miRs exhibit dysregulated expression in primary cancer specimens compared to tissues from healthy patient populations, including miR-21, miR-125b, miR-143, miR-145, miR-10b, miR-26a, miR-155 and miR-301 (27, 28). [score:3]
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46
[+] score: 3
We use bioinformatics analyses to screen SDF-1 targeting miRNAs, e. g. miR-301a, miR-301b, miR-3666, miR-130a, miR-130b, miR-4295, miR-454, etc. [score:3]
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[+] score: 3
For example, Lee EJ 2007 et al. [44] showed that the miRNAs miR155, miR21, miR222, Let7, miR376a, miR301, miR100, miR125, miR142 and others are overexpressed significantly in human PC. [score:3]
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[+] score: 3
With the application of in situ RT-PCR, Lee et al. showed that the aberrantly expressed miR-221, miR-301 and miR-376a were localized to pancreatic cancer cells but not to stroma or normal acini or ducts. [score:3]
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[+] score: 3
In breast cancer, PTEN is targeted by miR-29b (94) and miR-301 (95). [score:3]
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50
[+] score: 2
Hence, our results are in agreement with the Lu et al. study suggesting that the miR-301/miR-130 family positively regulates NF-κB signaling. [score:2]
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[+] score: 2
For example, we found significant overexpression of miR-103, miR-107, miR-301 and miR-338 in lung cancer cells as compared to HBECs. [score:2]
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[+] score: 2
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-138-1, rno-mir-138-1, hsa-mir-760, rno-mir-301b, rno-mir-760
Other genes relevant to gene regulation include epigenetic modulators (e. g. Hira, Ehmt2, Yeats2), miRNAs (e. g. Mir138-1, Mir760, Mir301b) and 16 zinc finger transcription factor genes (e. g. Zfp105, Zbtb8a, Zbtb8b, Zdhhc17). [score:2]
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[+] score: 2
For the hub genes, shown in Table  1, four pairs were identified at FDR < 0.05, including ALDH1L1 and hsa-miR-342-5p (r = −0.27, FDR = 1.76E-03), NAALAD2 and hsa-miR-140-3p (r = −0.29, FDR = 7.98E-04), ORMDL3 and hsa-miR-362-3p (r = −0.20, FDR = 3.23E-02), and PCCA and hsa-miR-301b (r = −0.25, FDR = 5.42E-03). [score:1]
GeneGene-level p-value [a] GS GS p-value MM MM p-valueRank [b] miRNA r [c] p-value FDR GPD1L 2.67E-02 −0.23 1.06E-03 0.90 1.29E-71 1 hsa-miR-210 −0.17 7.37E-03 7.91E-02 CCDC50 2.12E-02 −0.20 4.68E-03 0.85 6.79E-58 2 hsa-miR-501-3p −0.19 3.93E-03 5.05E-02 NAALAD2 8.05E-03 −0.24 5.76E-04 0.85 1.47E-57 3 hsa-miR-140-3p −0.29 1.97E-05 7.98E-04 ALDH1L1 4.94E-03 −0.28 7.13E-05 0.85 3.15E-57 4 hsa-miR-342-5p −0.27 5.13E-05 1. 76E-03 ADH1B 3.14E-02 −0.27 8.82E-05 0.85 4.39E-56 5 — — — — ADH1A 5.00E-02 −0.26 1.83E-04 0.82 2.34E-50 6 hsa-miR-590-3p −0.09 1.06E-01 4.46E-01 PCCA 2.38E-02 −0.21 2.68E-03 0.82 3.87E-49 8 hsa-miR-301b −0.25 2.08E-04 5.42E-03 ORMDL3 3.87E-03 −0.29 3.04E-05 0.80 3.29E-45 9 hsa-miR-362-3p −0.20 2.12E-03 3.23E-02EPB41L4B [d] 7.42E-05 −0.29 3. 47E-05 0.67 2.63E-27 28 has-miR-3613-3p −0.11 6.46E-02 3.4E-01GS, gene significance; MM, module membership. [score:1]
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[+] score: 1
In the Figure, the red arrows (for miR-19a-3p, miR-28-5p and miR-301-3p) indicate these sequences are mapped to the genome sequence with one mismatch. [score:1]
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57/30.85/5.71 Yes 20 64/58 0 (0) hsa-mir-130a-3p 5/5/0 0.76/0.97/0 Yes 56 724/172 27 (3.73) hsa-mir-151a-3p 6/6/3 2.87/1.26/0.48 Yes 49 76/77 3 (3.95) hsa-let-7d-3p 6/4/0 0.70/0.31/0 Yes 66 9/1 0 (0) hsa-mir-27b-3p* 5/0/0 0.25/0/0 Yes 64 921/8 2 (0.22) hsa-mir-301b-3p* 5/2/1 1.24/−/− No 63 NA NA hsa-mir-340-3p* 4/0/0 1.19/0/0 No 70 NA NA hsa-mir-377-3p* 4/3/0 8.10/4.6/0 No 54 NA NA hsa-mir-539-5p* 6/6/0 2.23/1.62/0 No 18 NA NA hsa-mir-889-3p* 5/5/0 0.62/0.41/0 No 62 NA NA hsa-mir-99a-5p 6/6/4 3.40/1.44/0.30 No 13 NA NA 22 miRNAs were found to be significantly hypoedited in GBM (wilcoxon-two-tailed, p < 0.05). [score:1]
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hsa-mir-301a and hsa-mir-301b [45] ranked third and ninth, respectively; they are pivotal oncogenes in human breast cancer and promote nodal or distant relapses through multiple pathways. [score:1]
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Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-98, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, 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-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-302c, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-328, hsa-mir-342, hsa-mir-326, hsa-mir-135b, hsa-mir-338, hsa-mir-335, hsa-mir-345, hsa-mir-424, hsa-mir-20b, hsa-mir-146b, hsa-mir-520a, hsa-mir-518a-1, hsa-mir-518a-2, hsa-mir-500a, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-92b, hsa-mir-574, hsa-mir-614, hsa-mir-617, hsa-mir-630, hsa-mir-654, hsa-mir-374b, hsa-mir-1204, hsa-mir-513b, hsa-mir-513c, hsa-mir-500b, hsa-mir-374c
Few FL-specific miRNAs included miR-9/9*, miR-301, miR-338, and miR-213 [51]. [score:1]
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In our set of C. elegans_human ≥70% homologs, the following do not have ≥7 nucleotides of continuous similarity at the 5′ end: cel-miR-57 with hsa-miR-99a and hsa-miR-100; cel-miR-236 with hsa-miR-141 and hsa-miR-200a; and cel-miR-266 with hsa-miR-25*, hsa-miR-301a and hsa-miR-301b. [score:1]
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We discovered pro-proliferative miRNAs (miR-9 [*], miR-93, miR-130a, miR-130b, miR-301, miR-302b, miR-302d, miR-363, miR-372, miR-373), and anti-proliferative miRNAs (miR-7, miR-124a, miR-192, miR-193a, miR-193b, miR-199a [*], miR-432 [*], miR-497, miR-506, miR-517c) in A2780 cells. [score:1]
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For example, six miRNA loci (hsa-mir-185, hsa-mir-1306, hsa-mir-1286, hsa-mir-649, hsa-mir-301b and hsa-mir-130b) are located within genomic region implicated in DiGeorge syndrome. [score:1]
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Mir-130b and miR-301 were not found to be significantly different in amplified samples by SAM analysis. [score:1]
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