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12 publications mentioning mmu-mir-501

Open access articles that are associated with the species Mus musculus and mention the gene name mir-501. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 105
Other miRNAs from this paper: mmu-mir-375
Figure 1(A) Kaplan-Meier curves, showing both tumor-free survival and patient overall survival, which were higher in the patients with pancreatic body/tail cancer than in those with pancreatic head cancer; (B) Bars representing the significantly lower expression of miR-501-3p and higher expression of miR-375 in pancreatic body/tail cancer compared with pancreatic head cancer, as assessed by qRT-PCR; (C) Kaplan-Meier curves, presenting tumor-free survival and overall survival were significantly lower in the patients with high miR-501-3p expression than those with low expression. [score:8]
But the significantly different expressed proteins were not predicted to be direct potential targets of miR-501-3p using open-source software. [score:6]
MiR-501-3p down-regulates the expression of E-cadherin. [score:5]
Furthermore, we manipulated the E-cadherin expression and found the enforced expression of E-cadherin could rescue the miR-501-3p effects in Panc-1 cells (Figure 4B). [score:5]
We also demonstrated that miR-501-3p promotes the invasiveness of PDAC cells, possibly via regulating the expression of E-cadherin. [score:4]
We verified the lower expression of miR-501-3p and higher expression of miR-375 in the pancreatic body/tail cancer tissues compared with the pancreatic head cancer tissues (Figure 1B). [score:4]
Taken together, our results indicate that the lower expression of miR-501-3p in pancreatic body/tail cancer might be associated with the higher expression of E-cadherin, and subsequently, a less invasive/metastasis phenotype compared with pancreatic head cancer. [score:4]
Panc-1/Luc cells were infected with lentivirus (Lv-miR-501-3p, Lv-miR-501-3p -inhibition, and Lv-control) at a multiplicity of infection of 2. Detailed information on the lentiviruses is provided in Supplemental Table 6. A subcutaneous tumor mouse mo del was established by subcutaneous implantation of 1 × 10 [7] cells into the backs of mice. [score:3]
Using immunohistochemistry analysis, we found significantly high and low expressed E-cadherin and miR-501-3p, respectively, in pancreatic body/tail cancers than pancreatic head cancers (Figure 4C). [score:3]
Low recurrence risk of pancreatic body/tail cancer correlates with low expression of miR-501-3p. [score:3]
Double-stranded oligonucleotides corresponding to the wild-type (WT-3′-UTR) or mutant (MUT-3′-UTR) miR-501-3p binding sites in the 3′-UTRs of the potential target genes were synthesized (GenePharma, Shanghai, China) and ligated into apsiCHECK™-2 Vector (Promega, Madison, WI, USA). [score:3]
MiR-501-3p mimics, inhibitors or their negative controls were purchased from Life Technologies, Darmstadt, Germany in order to positively or negatively influence the respective miRNA level. [score:3]
A cutoff value of miR-501-3p was then selected according to the receiver operating characteristic (ROC) curve and the low expression group showed significantly lower tumor recurrence rate (Supplementary Table 3) and higher tumor-free survival (Figure 1C) than the high expression group. [score:3]
There was a significant negative correlation between the expression of E-cadherin and miR-501-3p (r = –0.596, P = 0.015, Figure 4D). [score:3]
In correlation analysis (Supplementary Table 2), higher miR-501-3p expression was significantly correlated with poorer differentiation (r = 0.272, P = 0.030). [score:3]
In the orthotopic PDAC mo del, Lv-miR-501-3p group presented higher expression of E-cadherin in the tumor tissue than the Lv-control group (Figure 4E). [score:3]
Low expression of miR-501-3p in pancreatic body/tail cancer, contributing to a low risk of tumor recurrence. [score:3]
To reveal the underlying mechanism of miR-501-3p -induced invasion, an antibody microarray was used to analyze differential protein expression between Panc-1 cells transfected with either miR-501-3p mimics or its control (Supplementary Table 4). [score:3]
However, two miRNAs (miR-501-3p and miR-375) were significantly differentially expressed between the two subtypes. [score:3]
Panc-1/Luc cells were infected with lentivirus (Lv-miR-501-3p, Lv-miR-501-3p -inhibition, and Lv-control) at a multiplicity of infection of 2. Detailed information on the lentiviruses is provided in Supplemental Table 6. A subcutaneous tumor mouse mo del was established by subcutaneous implantation of 1 × 10 [7] cells into the backs of mice. [score:3]
MiR-501-3p down-regulates E-cadherin in pancreatic cancer. [score:3]
Furthermore, the expression of miR-501-3p was significantly associated with tumor-free survival (P = 0.012, risk ratio [RR] = 1.164, 95% confidential interval [CI] = 1.034-1.311) and overall survival (P = 0.008, RR = 1.186, 95% CI = 1.046-1.346). [score:3]
It indicates that miR-501-3p might be a potential biomarker for PDAC carcinogenesis or tumor development [14]. [score:2]
Furthermore, miR-501-3p possibly promoted cancer invasion via down -regulating E-cadherin, which is well known as a transmembrane protein localized to the adherence junctions of the epithelial cell basolateral surface that plays a key role in epithelial morphology maintenance. [score:2]
After that, the mice in the Lv-miR-501-3p and Lv-miR-501-3p -inhibition groups showed increased and decreased tumor growth, respectively, compared with those in the Lv-control group (Figure 3A). [score:2]
Previous study showed an overexpression of miR-501-3p in non-functioning pituitary adenomas [12], malignant melanoma [13], compared with normal tissues. [score:2]
In addition, the expression of miR-501-3p in tumor tissues was evaluated to confirm the efficiency of lentivirus infection (Supplementary Figure 1). [score:1]
Compared with the Lv-control group (n = 8), the Lv-miR-501-3p group demonstrated a higher tumor burden and faster tumor development (Figure 3C). [score:1]
Biological effects of miR-501-3p on PDAC cells. [score:1]
Two out of 6 mice had liver metastasis in the Lv-miR-501-3p group (Figure 3B), while no metastasis was found in the other two groups. [score:1]
Unlike miR-375, miR-501-3p has not yet been well studied in human cancers. [score:1]
Yet, E-cadherin as a well-studied one involved in cancer invasion has an interaction network with miR-501-3p (Supplementary Figure 3), and thus was chosen for further experiments. [score:1]
Taking the fold-changes and rank sum differences into consideration, miR-501-3p was the only candidate for further study with a P < 0.05, a fold-change of > 2 and the largest rank sum difference. [score:1]
The Lv-miR-501-3p group showed a significantly higher tumor burden (reflected by total flux) than the Lv-control group. [score:1]
The first tumor metastasis event was observed in the Lv-miR-501-3p group at 5 weeks after implantation (Figure 3C). [score:1]
Slides were prehybridized in a hybridization oven for 30 min in hybridization buffer with 500 μg/ml yeast tRNA, 50% formamide, 2 × SSC, 50 μg/ml heparin, and 0.1% Tween 20, with the pH adjusted to 6. The slides were then hybridized for 1 h with 200 nM double-digoxigenin LNA -modified probes (Exiqon, Vedbaek, Denmark) for miR-501-3p. [score:1]
In addition, from the clinical characteristics analysis, we found that high miR-501-3p expression maybe linked with poor tumor differentiation but not lymphatic metastasis. [score:1]
Our results demonstrated that miR-501-3p promoted PDAC recurrence after surgery. [score:1]
At the end of the experiment, a total of 3 mice had tumor metastasis, and 1 mouse had died in the Lv-miR-501-3p group. [score:1]
At 6 weeks, a mouse in the Lv-miR-501-3p group died, possibly due to a high tumor burden. [score:1]
MiR-501-3p promotes tumor development in subcutaneous and orthotopic PDAC mouse mo dels. [score:1]
Hsa-miR-501-3p-recombinant lentivirus and control vectors were constructed by GeneChem Corp. [score:1]
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[+] score: 24
Interestingly, when we directly compared gene expression profiles of the IR sample and the sham sample, we found that the DE genes (microRNAs and mRNAs) were associated with the Toll-like receptor signaling pathway in which miR-125b-5p and miR-501-3p were down-regulated at reperfusion stage, leading to the increased expression of their target Myd88, c-Fos and A20 (Fig 6). [score:10]
Particularly, miR-125b-5p and miR-501-3p are down-regulated and activate the Toll-like receptor signaling pathway in response to hepatic IR injury. [score:4]
The expression changes of mmu-miR-501-3p and Fos are negatively correlated. [score:3]
Two microRNAs miR-125p and miR-501-3p are down-regulated in IR injury when compared to the sham control. [score:3]
0148677.g006 Fig 6Two microRNAs miR-125p and miR-501-3p are down-regulated in IR injury when compared to the sham control. [score:3]
Realtime quantitative PCR of mmu-miR-501-3p and Fos involved in Toll-like receptor pathway. [score:1]
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[+] score: 13
NDMA stimulation increased the expression of the primary miR-501 transcript, and still increased mature levels even when a transcription inhibitor was present, suggesting that undergoes post-transcriptional regulation [42]. [score:6]
This regulation may be controlled by the structure of miR-501, as hairpin structural stability increases the production of the mature miRNA [22]. [score:2]
However, miR-501 still appeared to be structurally conserved due to a number of compensatory mutations (SCI = 0.95, covariance contribution = -0.24). [score:2]
Of all of the alignments, miR-501 had the lowest mean pairwise identity (91%) across primates, similar to the average pairwise identity between most human and mouse pre-miRNA (>90%) [19]. [score:1]
Predicted structure of miR-501 by miRDeep2. [score:1]
miR-501-3p. [score:1]
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[+] score: 11
The graph depicts the interacting genes identified from epistasis scan of miRNA miR-501 in chromosome 1 and chromosome 2. The graph shows all known gene interactions between the two loci where genes colored in yellow are from locus on chromosome 2 and green are from locus on chromosome 1. The red line shows the possible pathway for the regulation of miR-501. [score:2]
miR-181, miR-30b* and miR-874 are additional suggestive eQTL with significant genome-wide (α < 0.1) threshold after permutationSimilarly, on chromosome 8 we identified eQTL for three miRNAs (miR-486, miR487b and miR-501) in confidence interval 72–95 Mb. [score:2]
miR-181, miR-30b* and miR-874 are additional suggestive eQTL with significant genome-wide (α < 0.1) threshold after permutation Similarly, on chromosome 8 we identified eQTL for three miRNAs (miR-486, miR487b and miR-501) in confidence interval 72–95 Mb. [score:2]
In line with this observation, for the eQTL mapped on chromosome 8, two miRNAs (miR-501-3p and miR-486) were clustered with the ‘brown’ module while miR-487 was assigns to the ‘red’ module but had significant module membership with the brown module as well (P = 0.004). [score:1]
Figure S2 Interaction network accessed via IPA software for epistasis of miR-501. [score:1]
Interestingly, Cops5 in the Nfkb1 pathway possibly be associated with miR-501 via Tp53 (Additional file 1: Figure S2). [score:1]
Helicases like Ddx39, Ddx49, Cd97 and Upf1 were mapped within the confidence interval of miR-486, miR-487b and miR-501 on chromosome 8. Further, four helicases (Ddx50, Ascc3, Ddx21 and Dna2) were mapped within the confidence interval of the eQTL controlling miR-126. [score:1]
We also found multiple SNPs on chromosome 2 (13–17 Mb) statistical interacting with SNPs on chromosome 1(3–11 Mb) for miR-501. [score:1]
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[+] score: 7
For example, miR-501 targets HBXIP (44), and miR-372/373 targets NFI/B (45). [score:5]
Jin J. Tang S. Xia L. Du R. Xie H. Song J. Fan R. Bi Q. Chen Z. Yang G. MicroRNA-501 promotes HBV replication by targeting HBXIPBiochem. [score:2]
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[+] score: 7
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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, 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, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Six miRNAs showed a trend for a stronger upregulation during the brown adipocyte differentiation - miRPlus_17856, mmu-miR-381, mmu-miR-501-3p, mmu-miR-21*, mmu-miR-296-5p and miRPlus_17832. [score:4]
Mir-136 and mir-718 were not detectable in the adipocyte cultures using the Taqman assays-on-demand, while mir-346, mir-298, mir-330 and mir-501 were expressed at low levels (Ct levels above 33), see Table 1. This suggests that currently there is no gold standard method (when RNA is limiting) to validate miRNA data profiles. [score:2]
5 miR-298 33.2 ±0.2 33.8 ±0.2 33.5 ±0.6 33.5 ±0.4 miR-346 35.7 ±1.1 36.4 ±0.8 35.7 ±0.6 34.7 ±0.4 miR-501 34.5 ±0.9 34.4 ±0.9 34.6 ±0.1 34.4 ±0.4 miR-718 ND ND ND ND miR-720 22.5 ±0.3 22.9 ±0.1 23.4 ±0.4 22.9 ±0. [score:1]
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[+] score: 6
For example, results were closer to Affymetrix results for miR-501-3p, which showed a clear up-regulation at day 12. [score:4]
miR-501-3p was selected on behalf of the group of miRNAs which gave controversial results with the two platforms, while miR-715 represented those miRNAs not detected as being regulated by either platform. [score:2]
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[+] score: 6
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]
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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[+] score: 5
Among these miRNAs, the expression of 10 miRNAs (miR337, miR714, miR346, miR500, miR101b, miR434, miR501, miR410, miR672 and miR425) was significantly decreased, and we therefore did not further examine the expression levels of these molecules by using quantitative RT-PCR (qRT-PCR). [score:5]
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[+] score: 5
miRNA RQ Validated target genes Biological process Role in disease miR-31-3p 4.5 RhoA Proliferation and migration Cancer 53 miR-691 3.4 No data No data No data miR-700-3p 3.1 No data No data No data miR-29a-5p 3.1 No data No data Cancer 54 miR-501-3p 3 Gria1 Neuro-transmision No data 55 miR-338-3p* 2.7 Aatk, Atp5g1, CoxIV Axonal guidance, apoptosis, mitochondrial function Cancer, neurodegeneration 42, 56 miR-139-3p 2.7 MMP11 Extracellular matrix organization Cancer 57 miR-34a-5p* 2.5 Bcl-2, Notch1, Map2k1, Sirt1 Apoptosis, mitochondrial function, oxidative stress response Cancer, Alzheimer, cardiomyopathy 29, 30, 34, 43, 44 miR-335-3p 2.1 Ank3 No data No data 58 miR-1949 1.7 Rb1 Cell cycle control Cancer 59 miR-326-3p 0.5 Bcl-xl, Notch1/2 Apoptosis, proliferation Cancer 60, 61 miR-671-5p 0.3 Smarcb1 Proliferation Cancer 62 miR-503-3p 0.2 No data No data No data miR-350* 0.2 p38, Jnk Apoptosis Cardiac hypertrophy 32 [*]miRNAs selected for further studies. [score:5]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-134, mmu-mir-204, mmu-mir-223
For instance, in the miRNA‐mediated synaptic plasticity regulating pathway, miR501 (Hu et al., 2015), miR223 (Harraz et al., 2012) and miR134 (Jimenez‐Mateos et al., 2012) target GluR1, GluR2 and NR2B, and DHX36, respectively. [score:4]
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[+] score: 3
The most highly expressed UniPR1331 -induced miRNAs (RQ> 20) were hsa-miR-616-3p and hsa-miR-15a-3p whereas the most UniPR1331-reduced miRNAs (RQ < 0.02) were hsa-miR-593-3p, hsa-miR-144-5p, hsa-miR-501-3p, hsa-miR-326 and hsa-miR-199a-3p. [score:3]
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