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24 publications mentioning mmu-mir-331

Open access articles that are associated with the species Mus musculus and mention the gene name mir-331. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 323
This down-regulation of miR-331-3p removes suppression of expression on several key downstream targets within the RAS activated and other pathways, which further contribute to disease progression. [score:12]
Building on our previous studies whereby we identified miR-331-3p as a tumor suppressor miRNA [21, 22], we propose that loss of miR-331-3p expression in PCa is an indicator of advanced disease and has downstream effects on targets within RAS activated pathways, further contributing to disease progression. [score:11]
We identified several new targets for miR-331-3p, one of which, RALA, is a direct target, is downregulated by miR-331-3p in PCa and is an important regulator of PCa growth. [score:10]
Ingenuity Pathway Analysis [®] (Ingenuity System, Inc) and TargetScan (Version 7.1: June 2016) were used to provide metadata on putative miR-331 target genes downregulated by miR-331-3p in the microarray. [score:8]
Transient overexpression of miR-331-3p significantly downregulated induced luciferase activity in C4-2B and LNCaP cells, indicating targeting of the RALA and PLCγ1 3’-UTRs by miR-331-3p (Figure 3D; LNCaP data not shown). [score:8]
The expression of miR-375, a known epigenetically regulated miRNA [67], was increased significantly by methylation and acetylation inhibition, while the expression of miR-331-3p remained unchanged. [score:8]
We identified an inverse correlation between intratumoral miR-331-3p expression and the clinico-pathologic features of PCa; including Gleason score, tumor stage, ratio of positive to negative lymph nodes and PSA level; suggesting that high tumoral miR-331-3p expression may be beneficial with regards to disease severity (Table 1). [score:7]
The smaller circle indicates the 25 samples in which miR-331-3p is downregulated, with significant absolute fold changes (<1.5 fold) visually annotated by difference in size and colour gradient within this downregulated subset. [score:7]
These features combined contribute to the lack of rescue of the mutated PLCγ1 target, and our conclusion that PLCγ1 is an indirect target of miR-331-3p. [score:6]
Figure 3 (A) Heat map of all significantly down regulated targets in a microarray study using LNCaP cells transiently expressing miR-331-3p. [score:6]
miR-331-3p expression is significantly downregulated in prostate tumors. [score:6]
Taken together, these data indicate that miR-331-3p is a tumor suppressor in PCa, whereby due to it's frequent downregulation, it is associated with a more aggressive clinical phenotype at the outset. [score:6]
Our in vivo studies provide robust evidence that replacement of miR-331-3p inhibits PCa growth, consistent with its loss from tumor tissue, and its designation as a tumor suppressor. [score:5]
Our results lead us to conclude that loss or reduction of miR-331-3p expression in PCa is a common finding and is an indicator of aggressive disease. [score:5]
Cohorts from The Cancer Genome Atlas (TCGA) consisting of varying numbers of prostate cancer patients (see Tables 1, 3, 4 and 5) were analysed by comparing expression of miR-331-3p in tumor tissue vs normal adjacent benign prostate tissue and correlation coefficients of intratumoral RALA, PLCγ1 or miR-331-3p expression (prostate cancer) relative to clinicopathologic features of Gleason score, tumor stage, ratio of positive lymph nodes and PSA values [73]. [score:5]
Thus inhibiting AKII should produce a significant impact on RALA, as it will reduce its functional capacity, and if combined with miR-331-3p it would reduce its tumor level of expression as well. [score:5]
Expression of each of the candidate miR-331-3p targets was evaluated in the 46 PCa cases above, with special attention focused on a subset of samples that indicated the largest change in miR-331-3p expression between a non-malignant adjacent tissue sample and its matched tumor sample. [score:5]
Consistent with these results, AKi-II significantly inhibited in vitro colony formation and in addition enhanced the inhibitory activity of miR-331-3p or si-RALA treatments on colony formation (Figure 5D and 5E). [score:5]
Fold decrease of candidate miR-331-3p target genes from microarray analysis and RT-qPCR detection of the same genes from LNCaP PCa cells overexpressing miR-331-3p. [score:5]
These studies demonstrate that miR-331-3p is a tumor suppressor miRNA in PCa and that its loss is associated with a more aggressive disease phenotype. [score:5]
While our mo del clearly shows that RALA is down regulated with transient miR-331-3p over expression, miR-331-3p also contributes to the down regulation of multiple other transcripts within the cell, as evidenced by our microarray data. [score:5]
Both of the RALA 3’-UTR target sequences display complementarity with a seven base pair region (7mer-m8; indicates perfect complementarity between base 2-8 of the seed region [58]) using TargetScan (Release 7.0: August 2015) [59], while the single PLCγ1 miR-331-3p seed region displays a six base pair region, followed by an A (7mer-1A; [58]). [score:5]
Specifically, miR-331-3p targets RALA directly reducing its effects on proliferation, migration and tumor growth of PCa cells. [score:4]
Mutation of the candidate miR-331-3p seed sites within the 3’UTR of RALA were nt 1587 CCAGGGG to GGTCCCC and nt 2628 CCAGGGG to GGTCCCC of the complete cDNA sequence; and 3’-UTR of PLCγ1 were nt 612 CAGGGG to GTCCCC (TargetScan Release 7.0: August 2015). [score:4]
Additional analysis of data from Taylor et al [73] similarly identified that miR-331-3p was significantly down regulated in tumor tissue relative to normal adjacent benign prostate tissue (Table 3) and that RALA expression was positively correlated with Gleason Score (Table 5). [score:4]
RALA is a direct target of miR-331-3p in PCa cells. [score:4]
php) [69] and DAVID (The Database for Annotation, Visualization and Integrated Discovery) [70, 71] were used to determine the pathway targets and cellular functions of genes down regulated by miR-331-3p, with corresponding figures produced by PathDesigner [®]. [score:4]
What could be the mechanism for the downregulation of miR-331-3p in PCa? [score:4]
Therefore, examination of this region for loss or disruption in PCa may provide insight for the down regulation of miR-331-3p expression in our patient sample set. [score:4]
In contrast, mutation of a single conserved miR-331-3p seed site in the 3’-UTR of PLCγ1 did not rescue miR-331-3p effects, suggesting that miR-331-3p activity is either indirect or mediated by alternative seed regions in LNCaP cells (data not shown). [score:3]
This RT-qPCR analyses indicated that the expression of RALA, PLCγ1, MARCKS and RRBP1 were negatively correlated with that of miR-331-3p in all samples from this subset (Figure 3C). [score:3]
miR-331-3p inhibits PCa xenograft tumor growth. [score:3]
Given that Aurora Kinase Inhibition could potentially work synergistically with miR-331-3p to inhibit signaling in the Ras-RALA pathway, we next investigated the effects of AKi-II treatment on PCa cells viability. [score:3]
** indicates previously reported targets of miR-331-3p in PCa. [score:3]
Focusing on the miR-331-3p target RALA, we assessed the proliferative capacity of PCa cells following siRNA -mediated degradation of RALA. [score:3]
Xenografts of 22Rv1 PCa cells transiently overexpressing miR-NC or miR-331-3p on NOD/SCID (NSG) mice. [score:3]
Pie graph representation of miR-331-3p expression across a large cohort study of 46 patient tumor samples with matched non-malignant control samples. [score:3]
Most significantly, when miR-331-3p is combined with existing inhibitors of RAS activated pathways, such as the AKi-II, the combination further reduces in vivo PCa tumor growth suggesting a new potential combinatorial approach for treating CRPC. [score:3]
As previously observed (Figure 2A), transient overexpression of miR-331-3p in 22Rv1 cells delays the initial detection and subsequent growth of xenografts in comparison to that of control miR-NC transfected cells (Figure 6A; blue vs green). [score:3]
Effects of miR-331-3p over expression on proliferation, migration, colony formation and xenograft growth. [score:3]
Correlation coefficients of intratumoral miR-331-3p expression (prostate cancer) relative to clinicopathologic features from The Cancer Genome Atlas (TCGA). [score:3]
Here, we describe two new miR-331-3p targets in PCa, RALA and PLCγ1, which are downstream of RAS in the RALGEF/RAL and PKC activation pathways. [score:3]
These results indicate that transient over expression of miR-331-3p significantly reduced 22Rv1 xenograft growth and that this was associated with increased survival. [score:3]
We chose an AKi-II so that we could further inhibit the RAL signaling pathway and determine if we could augment the miR-331-3p -induced reduction of tumor growth. [score:3]
miR-331-3p expression is reduced in PCa tissue relative to a paired non-malignant adjacent tissue (NAT). [score:3]
Clustering, volcano and scatter plots showing the distribution of differential gene expression induced by miR-331-3p, were produced from normalized data using the R ‘graphics’ package [72]. [score:3]
Identification of miR-331-3p target genes. [score:3]
Overall, these data suggest combining miR-331-3p with an AKi-II will result in increased tumor suppression in vivo and supports our previous in vitro observations. [score:3]
Effects of Aurora Kinase inhibitor II treatment of PCa cells +/- RALA and miR-331-3p. [score:3]
MRI revealed that AKi-II treatment of control miR-NC transfected cells significantly reduced the volume of resulting xenografts (not shown), while AKi-II co-treatment further enhanced the inhibitory effects of miR-331-3p transfection on the volumes of the resulting xenografts (Figure 6B). [score:3]
Figure 2Xenografts of 22Rv1 PCa cells transiently overexpressing miR-NC or miR-331-3p on NOD/SCID (NSG) mice. [score:3]
Further, we demonstrate synergistic PCa growth suppression with a combination of miR-331-3p and an AKi proving a new potential therapeutic avenue in CRPC. [score:3]
Mutation of two candidate miR-331-3p seed sites within the 3’-UTR of RALA significantly rescued miR-331-3p induced repressor activity, indicating a direct interaction between miR-331-3p and the RALA 3’-UTR (Figure 3D, 3E). [score:3]
To evaluate the functional effects of miR-331-3p as a putative tumor suppressor in PCa cells, we initially transiently overexpressed miR-331-3p in DU145 PCa cells and found it reduced proliferation (Supplementary Figure 3A), migration (Supplementary Figure 3B) and colony formation (Supplementary Figure 3C). [score:3]
All targets are represented with or without a predicted miR-331-3p seed region. [score:3]
Our findings above were further validated when we interrogated The Cancer Genome Atlas (TCGA) PCa tissue samples for expression of miR-331-3p. [score:3]
The 2 [-ΔΔCt] method was used to determine mature miR-331-3p or miR-375 expression relative to RNU6B small nuclear RNA (snRNA) [66]. [score:3]
RALA and PLCγ1 3’-UTRs are targeted by miR-331-3p. [score:3]
Pretreatment of LNCaP cells with miR-331-3p increased their sensitivity to the AKi-II by ˜57%, suggesting that miR-331-3p targets may be involved in pathways specific to the AKi-II (Figure 5C). [score:3]
We found that an AKi-II was a potent inhibitor of PCa cell growth, and when combined with miR-331-3p further reduced PCa growth in vivo. [score:3]
Our studies support this notion, where we were able to get the greatest suppression of tumor growth in vivo when miR-331-3p pre-treatment was combined with AKi-II treatment. [score:3]
miR-331-3p expression is colour indicated, where red is significantly increased by > 1.5 fold, green is significantly decreased by > 1.5 fold and grey is unchanged. [score:3]
Included in this cohort were ERBB-2 and DOHH, two targets of miR-331-3p we have described previously [21, 22]. [score:3]
Effects of Aurora kinase inhibitor II treatment of PCa cells +/- RALA and miR-331-3p. [score:3]
We next transiently overexpressed miR-331-3p in 22Rv1 cells and transplanted them into NSG mice and noted that miR-331-3p delayed the detection of palpable tumors in NSG mice from day 23 to day 25 compared to miR-NC transfected controls (Figure 2A). [score:2]
We found 148 genes down regulated by at least 1.5 fold in samples treated with pre-miR-331-3p (Figure 3A; Supplementary Table 2). [score:2]
To identify the major pathways and genes regulated by miR-331-3p in PCa, we performed microarray analysis of LNCaP cells treated for 24 h with pre-miR-331-3p or pre-miR-NC. [score:2]
Our data contributes to this rapidly growing library of signatures wherein the down regulation or loss of miR-331-3p in PCa appears to contribute to progression and/or phenotype of PCa. [score:2]
Furthermore, across all specimens, a global down regulation of miR-331-3p within the tumor samples relative to nonmalignant prostate was observed (Figure 1D), and 11 of these cases showed divergent miR-331-3p levels in the tumor and matched non-malignant adjacent tissue (NAT) (Supplementary Figure 1A). [score:2]
miR-331-3p; miR-642-5p; miR-7-5p) to regulate the activity of the PI3K/AKT and other pathways in a number of cancer types, including PCa [17– 23]. [score:2]
In contrast, only 4 of 12 mice injected with miR-331-3p transfected 22Rv1 cells had reached this end point at day 40. [score:1]
Effects of miR-331-3p and AKi-II pre-treatment of PCa cells on xenograft growth. [score:1]
We observed that the primary miR-331 transcript was down regulated in a tumor sample compared to a matched non-malignant sample, which resulted in depleted miR-331-3p maturation. [score:1]
In a pilot cohort of matched nonmalignant prostate vs prostate tumor samples from patients with similar clinical characteristics (age, preoperative PSA, lymph node involvement, Gleason grade), 9 of the 11 samples (81%) exhibited at least a 1.5 fold decrease in miR-331-3p expression in tumor tissue relative to non-malignant prostate (Odds Ratio = 4.5; Figure 1A). [score:1]
Synthetic miRNA precursor (pre-miR) molecules corresponding to human miR-331-3p (pre-miR-331-3p; Product ID: PM10881), miR-375 (pre-miR-375; Product ID: PM10327) and a negative control miRNA (pre-miR-NC; Negative Control #1, Product ID: AM17110) were sourced from Ambion (Thermo Fisher Scientific). [score:1]
The effects of miR-331-3p and AKi-II pre-treatment of PCa cells on 22Rv1 xenograft growth. [score:1]
In this cohort, miR-331-3p was down regulated in 33/46 prostate tumor samples when compared to the matched nonmalignant prostate, with 25 of 46 patients (˜55%) showing a 1.5 fold or greater decrease (Figure 1B, 1C). [score:1]
Our observations are consistent with those of Jeon et al, and we propose that the miR-331-3p induced reduction of RALA in our cancer mo dels is cyto “destructive” and anti-migratory. [score:1]
AKi-II pretreatment also reduced xenograft growth, with either AKi-II or miR-331-3p treatments reaching similar tumor volumes at the time of first cull in the miR-NC treated group (Figure 6A). [score:1]
There are a small number of reports that implicate miR-331-3p in the progression or phenotype of PCa [39– 41]. [score:1]
Figure 6 (A) miR-NC and miR-331-3p (+/- AKi-II; 10μM) xenograft NSG mice were monitored over a 33 day period for tumor size and volume. [score:1]
Finally, in miR-NC transfected cell xenografts, tumor volume end points were reached only 4 days after the first cull event, with miR-331-3p transfected cell xenografts taking significantly longer to reach end point at approximately 10 days post first cull (Figure 6C). [score:1]
Two days later (Day 12 post first cull), AKi-II treated (miR-NC transfected) cell xenografts reached end points with the miR-331-3p and AKi-II co -treated group taking the longest to reach end point (extending out to 14 days post first cull) (Figure 6C). [score:1]
Herein, we also show that the efficacy of AKi-II treatment may be improved by introduction of miRNAs, as the introduction of miR-331-3p pre-treatment in combination with AKi-II treatment has lasting effects on in vitro cell proliferation and colony formation, and most importantly, PCa cell xenograft growth. [score:1]
Using the Bliss Independence Mo del [74], the combination treatment of cells with miR-331-3p and the AKi-II (Supplementary Table 3) or with si-RALA (Supplementary Table 4) was found to be synergistic in both cases (Figure 5D; Figure 5E ). [score:1]
This was opposed to the previous in-vitro result using miR-331-3p (Figure 5D) or si-RALA (Figure 5E) in combination with the AKi-II, where we observed a synergistic effect. [score:1]
Log-rank (Mantel-Cox) and Gehan-Breslow-Wilcoxon testing revealed the survival of miR-331-3p treated mice was significantly different to miR-NC treated mice (p<0.0001; p<0.0002). [score:1]
The miR-331 gene is situated at chromosomal locus 12q22. [score:1]
For microarray analysis, total RNA was isolated from LNCaP cells 24 h following transfection with 30 nM pre-miR-331-3p or pre-miR-NC. [score:1]
Hence, the effects of miR-331-3p on PCa proliferation and migration, are in part, mediated by RALA and/or the RALGEF/Ral activation pathways in PCa cells. [score:1]
Figure 1 (A) Taqman qRT-PCR detection of miR-331-3p in tumor samples (red bars) relative to a matched non-malignant control sample (green bars) in a pilot cohort study. [score:1]
RALA and PLCγ1 are new targets of miR-331-3p in PCa as determined by bioinformatics, microarray detection, and investigating of a non-malignant vs tumor cohort study. [score:1]
Here, we sought to investigate whether the observed absence of miR-331-3p in PCa- was due to either DNA methylation or histone deacetylase inhibition and we determined that this was not the case, when compared with a known miRNA, miR-375, whose epigenetic regulation in PCa has been well studied and is transcriptionally repressed via epigenetic mechanisms [67, 45]. [score:1]
Analysing this data using the Bliss Independence Mo del [74], the combination treatment of the AKi-II with miR-331-3p was found to have an additive effect (Supplementary Table 5). [score:1]
RNA was harvested and used for Taqman RT-qPCR detection of miR-331-3p, miR-375 and RNU6B, as described above. [score:1]
Of these 148 genes, 81 (54.7%) contained miR-331-3p seed regions within their 3’-UTR (p ≤ 3.3 × 10 [-8]) based on DAVID and DIANA miR-ExTra analyses. [score:1]
22Rv1 cells were transfected as described above with pre-miR-331-3p or pre-miR-NC (50 nM). [score:1]
To evaluate the effects of combining the AKi-II with miR-331-3p in vivo, we established xenografts of miR-331-3p overexpressing 22Rv1 cells that were treated ± Aki-II. [score:1]
Introduction of miR-331-3p into PCa cells reduces in vitro and in vivo tumor growth. [score:1]
Average miR-331-3p levels across malignant and adjacent normal prostate tissue in two publicly available cohorts. [score:1]
This suggested that there was potentially a -pretranscriptional- modification of the primary miR-331 transcript, and ruled out the abnormal maturation of miRNA pathway hypothesis. [score:1]
Log-rank (Mantel-Cox) testing of all survival curves revealed the survival of AKi-II, miR-331-3p and combination treated mice was significantly different to miR-NC treated mice (p<0.0005), with a Logrank test for trend revealing a significant trend (p<0.0011). [score:1]
miR-331-3p has been associated with chronic and acute lymphoblastic leukemia where it has been described by several separate groups as a potential therapeutic candidate [36– 38]. [score:1]
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2
[+] score: 45
To explore the functional link between altered miRNA expression and AD development, we predicted the potential targets of two representative miRNAs, miR-331-3p and miR-409-5p, which were the top -elevated and top-reduced miRNAs in both groups, by three prediction methods (miRDB, miRanda and TargetScan). [score:8]
It's possible that miR-331-3p, by regulating the expression of its target genes, promotes the pathogenesis of AD in the context of increased Aβ level. [score:6]
MiR-331-3p and miR-409-5p were predicted to each target 1138 and 745 genes (that are predicted in all three methods), Further analysis using GO database showed that the top biological processes affected by the predicted target genes are phosphate metabolic process and regulation of transcription (GO:0006796 and GO:0045449). [score:6]
It's note-worthy that the level of miR-331-3p becomes lower in AD brains at 12 months of age, possibly reflecting a negative-feedback mechanism linking the degree of AD disease with miR-331-3p expression level. [score:5]
In other systems, miR-331-3p was found to be up-regulated in acute and chronic lymphocytic leukemia and colorectal cancer [26], [27]. [score:4]
It's possible that cellular changes in late-stage AD surpasses the accumulation of Aβ in regulating miR-331-3p expression level. [score:4]
The expression of miR-331-3p may be regulated by genes involved in cell cycle control, such as E2F1, SOCS1, and genes involved in carcinogenesis and myogenesis [27]– [30]. [score:4]
The other 5 miRNAs all showed significant alterations in expression levels at 9 months of age, but these alterations became either not significant (miR-331-3p, miR-7a-5p, miR-501-3p and miR-434-3p) or reversed (miR-7b-5p) at 12 months of age. [score:3]
Such alteration was not observed by comparing AD and WT mice at 4 months of age, but begins to emerge at 6 months of age when Aβ deposition starts, indicating that the dysregulation of miR-331-3p may stem from the accumulation of Aβ in AD brains. [score:2]
Similar to miR-331-3p, some miRNAs such as miR-99b-5p, miR-100, miR-7b-5p and miR-501-3p also have a reversed expression change at late stage of AD (12 months) compared with those at relatively early AD stages (6 to 9 months). [score:2]
Among them, nine miRNAs (miR-99b-5p, miR-7b-5p, miR-7a-5p, miR-501-3p, miR-434-3p, miR-409-5p, miR-331-3p, miR-138-5p and miR-100-5p) showed consistent changes in both groups. [score:1]
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3
[+] score: 17
We also observed significant inhibition of immunostimulatory ssRNA sensing by select LNA/DNA phosphorothioate AMOs from Classes 3 and 4. Although miRNA -based mechanisms could be at play for LNA/DNA AMOs targeting abundant miRNAs (such as miR-191-5p, miR-16-5p, miR-29a-3p or miR-100-5p), such effects can be ruled out for other AMOs of Class 3 targeting poorly abundant miR-224-5p, miR-331-3p, miR-134-5p or miR-31-5p. [score:7]
Next, dose-response studies comparing the activity of highly inhibitory AMOs (miR-182-5p 2′OMe and miR-331-3p LNA/DNA) and that of poorly inhibitory AMOs (miR-224-5p 2′OMe and miR-195-5p LNA/DNA) on both TLR7 and TLR8 sensing were conducted in human PBMCs (Figure 3C and D). [score:5]
Noteworthy, select AMOs from Classes 1 and 3 (which did not significantly affect TNF-α production in BMMs) significantly reduced TNF-α production, suggesting a specific TLR8 inhibitory activity of these sequences (e. g. 2′OMe AMOs for miR-146a-5p or miR-331-3p). [score:3]
In line with a predominant TLR7 inhibitory effect of LNA/DNA AMOs, the miR-331-5p LNA/DNA AMO significantly decreased IFN-α levels compared to the miR-195-5p LNA/DNA AMO, while having a smaller impact on TLR8 -driven TNF-α production (Figure 3D). [score:2]
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4
[+] score: 13
We identified two upregulated miRNAs, namely miR-494 and miR-695 and six downregulated miRNAs, namely miR-331, miR-467b, miR-467f, miR-1195, miR-101b and miR-690 with statistical significance (p<0.05). [score:7]
In contrast to the microarray data, expression of miR-101 and miR-467f increased as observed by qRT-PCR, showing discrepancy between the two methods (Figures 2C and E), and miR-331 showed no significant change in expression (Figure 2F). [score:5]
Cells were treated with 2 or 20 ng/ml of TNF-α for 2 h or 4 days and the expression of miR-494, miR-690, miR-101b, miR-467b, miR-467f and miR-331 was measured by qRT-PCR. [score:1]
[1 to 20 of 3 sentences]
5
[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
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6
[+] score: 8
Mir-29a, miR-219, miR-338 and miR-132 were the miRNAs undergoing the strongest upregulation during development, a result confirmed by reverse transcription PCR (Supplementary Fig. 1) and in agreement with previous data 8, whereas miR-298, miR-149 and miR-331 were the top downregulated miRNAs. [score:8]
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7
[+] score: 7
Liu XH LncRNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancerMol. [score:4]
LncRNA HOTAIR, playing an oncogenic role in gastric reported by Liu et al [15], acted as a ceRNA that modulated the expression of human epithelial growth factor receptor 2 (HER 2) through working as a sink of miR-331-3p. [score:3]
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8
[+] score: 6
hsa-miR-331-5p has human tumor suppressor role in prostate cancer, leukemia, gastric cancer, liver cancer, Parkinson's disease, and so forth [36, 37]. [score:5]
hsa-miR-mit-1 has shown one hit with human miRNA hsa-miR-331-5p with 59 score and 4.9 E-value. [score:1]
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9
[+] score: 6
These disease -associated miRNAs are also listed in Table 1. In addition, we detected a trend in the up-regulation of the following miRNAs, although the values were not consistent enough to meet the criteria that 5 of the 6 infected mice show a fold change >1.75; miR-200a, miR-200b, miR-26a, miR-186, miR-331-3p, miR-152, miR-221. [score:6]
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10
[+] score: 6
Quantitative real-time PCR (qRT-PCR) analyses showed that the expression profiles of seven miRNAs (let-7a, miR-125a, miR-144, miR-2423, miR-3613-5p, miR-331* and miR-4028-3p) were consistent with the results from deep sequencing (Supplementary Figure S1). [score:3]
The expression patterns of seven known miRNAs (let-7a, miR-125a, miR-144, miR-2423, miR-3613-5p, miR-331* and miR-4028-3p) were successfully validated using qRT-PCR analyses. [score:3]
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11
[+] score: 5
Other miRNAs from this paper: mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
miR-331-3p promotes proliferation and metastasis of hepatocellular carcinoma by targeting PHLPP. [score:3]
MicroRNA-331-3p promoted proliferation and EMT -mediated metastasis of HCC via the suppression of PHLPP -mediated de-phosphorylation of Akt [20]. [score:2]
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12
[+] score: 5
Other miRNAs from this paper: mmu-mir-193a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-193b
Recently, miR-331-3p and miR-193a-3p might suppress ING5 expression to increase cell proliferation and decrease multi- chemoresistance respectively [12, 16]. [score:5]
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13
[+] score: 4
By contrast, no differentiated expression levels were observed in other miRNAs, such as miR-664-3p and miR-331-3p, in EV71-infected cells (Fig. 3A), which is consistent with the NanoString miRNA profiling results. [score:3]
The expression of miR-150-5p, miR-664-3p, miR-331-3p, and miR-876-5p was evaluated through qPCR. [score:1]
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14
[+] score: 4
Our results showed that the expression patterns of miR-1, miR-133a, miR-133b, miR-144, miR-206, miR-299, miR-331 and miR-4286 (Additional file 3: Figure S3) were significantly different in the three stages (p < 0.01), indicating that they may participate in the regulation of follicular transition. [score:4]
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15
[+] score: 4
Regulation of expression of deoxyhypusine hydroxylase (DOHH), the enzyme that catalyzes the activation of eIF5A, by miR-331-3p and miR-642-5p in prostate cancer cells. [score:4]
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16
[+] score: 4
Other miRNAs from this paper: mmu-mir-211
Similarly, HOTAIR may function as an completing endogenous RNA to regulate the expression of human epithelial growth factor receptor 2 (HER2) through sponging miR-331-3p [25]. [score:4]
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17
[+] score: 4
The differential miR pattern revealed five miRs that were >2-fold upregulated by TPO only in the presence of STAT5A/B: miR-193b, miR-132, miR-125a, miR-331-5p and miR-669a (Fig. 1a and ). [score:4]
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18
[+] score: 4
Other miRNAs from this paper: hsa-mir-107, mmu-mir-107, hsa-mir-331
Liu XH Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancerMol. [score:4]
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[+] score: 3
Out of a total of 847 miRs, 3 miRs presented as significantly up- (miR-181a*, miR-146a, miR-21) and 5 miRs as down-regulated (miR-133b, miR133a, miR331-3p, miR30c-2*, miR-204) in patients with AAAs compared to controls. [score:3]
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Additionally, prior studies from various mo dels of retinal degeneration identified over 300 differentially expressed miRNAs 63– 90, a total of 16 common miRNAs were identified (miR-1187, miR-125b-5p, miR-331-3p, miR466d-3p, miR-467f, miR-542-3p, miR-574-5p, miR654-3p, miR669h-3p, miR-882, miR-342-3p, miR-466a-5p, miR-466d-5p, miR-706, miR-345-3p, miR532-5p). [score:3]
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Similarly, longSAGE tags also suggest the expression of two human (mir-7-1 and mir-125a) and three mouse (mir-331, mir-351, and mir-495) miRNAs that have not been experimentally confirmed (Table 1). [score:3]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
Spinal cord miR-28, miR-217, miR-218-1, miR-329, miR-331. [score:1]
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In the setting of HCC, miR-222 [12], miR-21 [13], miR-106b [14] and miR-331-3p [15] have been reported to be tumor oncogene. [score:1]
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At 8 h after exposure injection, the level of 6 miRNAs (miR-451, miR-122, miR-350, miR-301a, miR-126, and miR-331) in the whole blood increased significantly. [score:1]
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