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28 publications mentioning mmu-mir-708

Open access articles that are associated with the species Mus musculus and mention the gene name mir-708. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 319
MiR-708 directly binds to 3’UTR of CD38MiRNAs can inhibit gene expression directly by binding to the target gene at the 3’UTR or indirectly by inhibiting multiple components in the signaling pathway [23, 24]. [score:11]
Using target prediction algorithms, we identified several miRNAs with potential CD38 3’UTR target sites and determined miR-708 as a potential candidate for regulation of CD38 expression based on its expression and regulation by TNF-α. [score:11]
The inhibition of PI3 kinase signaling by miR-708 involves induction of PTEN expression which is likely to have a significant impact on ASM cell proliferation and AHR, the latter through inhibition of expression of CD38 and potentially other pro-inflammatory genes. [score:9]
We report that miR-708 down-regulates CD38 expression through mechanisms that involve direct binding to the 3’UTR as well as indirectly by regulating JNK MAP kinase and PI3 kinase signaling in HASM cells. [score:9]
Mutation of four bases in the target sequence on the CD38 3’UTR reversed the inhibitory effect of miR-708 on luciferase activity confirming the specificity of its target binding at the 3’UTR of CD38 (Figure  3C). [score:8]
We also examined miR-708 expression and its effects on CD38 expression in ASM cells obtained from asthmatics to determine whether the augmented cytokine -mediated CD38 expression stems from altered regulation through miR-708. [score:8]
We further characterized miR-708 in HASM on the basis that its expression in HASM cells is regulated by the inflammatory cytokine rh-TNF-α, which is elevated during allergic asthma [40, 41], as well as its differential expression in cells from asthmatics versus non-asthmatics, and therefore its potential to regulate the expression of genes involved in signaling mechanisms regulating inflammation. [score:8]
miR-708 inhibits CD38 expression and its enzymatic activity in HASM cellsTo examine whether miR-708 alters the expression level of CD38, NA-HASM cells were transiently transfected with different concentrations of miR-708 mimic. [score:7]
In human ASM cells, TNF-α -induced CD38 expression is regulated by miR-708 directly binding to 3’UTR and indirectly by regulating JNK MAPK and PI3K/AKT signaling and has the potential to control airway inflammation, ASM contractility and proliferation. [score:7]
These results suggest that decreased JNK MAP kinase phosphorylation caused by increased expression of MKP-1 may be involved in miR-708 regulation of CD38 expression in HASM cells. [score:6]
Among the numerous potential CD38 3’UTR binding targets that we have identified, miR-708 and miR-140-3p [17] appear to play major roles in the regulation of CD38 expression in HASM cells. [score:6]
We investigated miR-708 expression, its regulation of CD38 expression and the underlying mechanisms involved in such regulation in human ASM cells. [score:5]
TNF-α caused a decrease in miR-708 expression in cells from non-asthmatics while it increased its expression in cells from asthmatics. [score:5]
To establish the specificity of the inhibitory effect of endogenous miR-708 on CD38 expression, NA-HASM cells were transfected with miR-708 mimic, scrambled sequence mimic or the antagomir of miR-708 mimic. [score:5]
Rh-TNF-α -induced CD38 expression following miR-708-antagomir transfection was similar to the expression in cells transfected with scrambled sequence mimic (Figure  2D). [score:5]
miR-708 inhibits CD38 expression and its enzymatic activity in HASM cells. [score:5]
An effect of miR-708 on PTEN expression is expected to profoundly affect cytokine -induced CD38 expression in ASM cells by modulating PI3 kinase signaling. [score:5]
Significant inhibition of CD38 expression was observed following transfection of miR-708 mimic at concentrations ≥ 50 nM (n = 3–5 donors). [score:5]
Since the target sites of these miRNAs are closely situated in the 3’UTR of CD38 transcript (see Figure  3A), we examined whether transfection of HASM cells with both miR-140-3p and miR-708 would amplify the inhibitory effect on enzymatic activity of CD38. [score:5]
Four bases in the target sequence on the CD38 3’UTR were mutated to establish specificity of miR-708 target binding (Figure  3A). [score:5]
Mutation of four bases (ctCgCCg) at the target site (AGCTCCT) specific for miR-708 was achieved using the QuikChange Lightning Multi Site-Directed mutagenesis kit. [score:5]
In the current study, we have shown that over -expression of miR-708 through transfection causes increased PTEN expression and an associated decrease in AKT phosphorylation. [score:5]
Prior studies have revealed a prominent regulatory role of miR-708 in the expression of phosphatase and tensin homolog (PTEN), which in turn regulates PI3 kinase signaling through activation of AKT [18]. [score:5]
In this study, we investigated the expression of miR-708, its potential additive role with miR-140-3p in the regulation of CD38 expression and the underlying mechanisms involved in such regulation in human ASM cells. [score:5]
In consistence with an overall attenuation of PI3 kinase signaling in miR-708 -mimic -transfected cells, there was a significant increase in PTEN expression compared to expression in cells transfected with the scrambled sequence mimic (Figure  7C). [score:4]
In summary, this study provides evidence for miR-708 regulation of CD38 expression in human ASM cells. [score:4]
Rh-TNF-α caused a significant reduction in miR-708 expression in growth-arrested NA-HASM cells compared with cells treated with vehicle (n = 8 donors), while it caused a significant increase in its expression in AS-HASM cells (n = 6 donors). [score:4]
In this study, we examined the effect of miR-708 transfection following TNF-α exposure (20 min) on levels of total MAP kinase protein as well as phosphorylated (activated) protein in order to determine whether decreased MAP kinase activation is an underlying mechanism in the regulation of CD38 expression. [score:4]
We also observed that transfection of cells with both miR-140-3p and miR-708 has no additive or synergistic effects on CD38 enzymatic activity, suggesting that either miRNA is capable of independently regulating CD38 expression in HASM cells. [score:4]
We first examined whether miR-708 regulates the expression of CD38 by directly binding to its 3’UTR by performing dual luciferase reporter assays in a heterologous cell system (NIH-3 T3 cells). [score:4]
In non-asthmatic HASM (NA-HASM) cells, rh-TNF-α caused a significant (p < 0.0001) reduction in the expression of miR-708 (Figure  1B) compared to expression in unstimulated (vehicle -treated) cells. [score:4]
Transcriptional regulation of CD38 expression by miR-708. [score:4]
Our study also shows that ASM cells obtained from asthmatics have increased constitutive as well as rh-TNF-α -induced expression of miR-708 compared to expression in cells from non-asthmatics. [score:4]
Dual luciferase reporter assays in NIH-3 T3 cells revealed regulation of expression by direct binding of miR-708 to CD38 3’UTR. [score:4]
Our previous studies have identified a role for miR-140-3p in the regulation of cytokine -induced CD38 gene expression and enzyme activity independent of miR-708 [17]. [score:4]
Figure 2 MiR-708 inhibits CD38 expression in HASM cells. [score:4]
Dual luciferase reporter assays were performed to determine whether miR-708 binds directly to CD38 3’UTR to alter gene expression. [score:3]
To examine whether miR-708 alters the expression level of CD38, NA-HASM cells were transiently transfected with different concentrations of miR-708 mimic. [score:3]
Note no significant change in expression of total or phosphorylated ERK (n = 5–6 donors) and p38 (n = 3–5 donors) following miR-708 mimic transfection. [score:3]
In contrast, rh-TNF-α exposure significantly increased the expression of miR-708 (p = 0.0098) in asthmatic-HASM (AS-HASM) cells (Figure  1C). [score:3]
Cells were transfected with miR-708 mimic or its scrambled sequence mimic, exposed to rh-TNF-α for 24 h and expression levels of the MAP kinases determined by analysis of cell lysates. [score:3]
Mutation of miR-708 target site and dual luciferase reporter assay. [score:3]
B and C : miR-708 expression in HASM cells from non-asthmatics (NA-HASM) and asthmatics (AS-HASM), respectively. [score:3]
Location of miR-708 target site at the 3’UTR of CD38 transcript is 21 bases away from the stop codon. [score:3]
Figure 1 Expression of miR-708 in rh- TNF-α -treated ASM cells. [score:3]
analysis of cell lysates following transfection with 50 nM miR-708 mimic (mimic) or scrambled mimic (scr) and treatment with rh-TNF-α for 20 min (for total and phosphorylated levels) or 24 h (for total expression levels) were performed with antibodies against phosphorylated and total ERK (A and B) as well as p38 (C and D), respectively. [score:3]
This finding was further confirmed in AS-HASM where miR-708 mimic at 50 nM significantly inhibited CD38 transcript level relative to the scrambled sequence mimic (Figure  2B). [score:3]
Our findings suggest the possibility that miR-708 can be used as a potential therapeutic strategy to inhibit ASM cell proliferation and contractility. [score:3]
Shown are the mutated bases in the miR-708 target site of the 3’UTR of CD38. [score:3]
Differential expression of miR-708 in HASM cells. [score:3]
Further, a significant reduction was also noted in the expression of AKT2 (Figure  7B), an isoform of AKT that has a 3’UTR binding site for miR-708 [25]. [score:3]
A and B: analysis of cell lysates following transfection with 50 nM miR-708 mimic (mimic) or scrambled sequence mimic (scr) was performed as described in Figure  5 to detect JNK MAP kinase after rh-TNF-α treatment for 20 min (total and phosphorylated levels) (n = 4 donors) as well as total JNK expression after rh-TNF-α treatment for 24 h (n = 3 donors). [score:3]
Co-transfection of HASM cell with miR-140-3p and miR-708 at 50 nM and 100 nM (equimolar concentrations) significantly inhibited CD38 enzymatic activity relative to cells transfected with scrambled sequence mimic. [score:3]
D : miR-708 expression in AS-HASM cells is higher than in NA-HASM cells both under vehicle and TNF-α -treated conditions (3–5 donors/group). [score:3]
The 3’ Untranslated Region (3’UTR) of CD38 has multiple miRNA binding sites, including a site for miR-708. [score:3]
Note significant attenuation of CD38 expression by miR-708 mimic transfection (n = 3 donors); C: ADP-ribosyl cyclase activity in AS-HASM (AS) and NA-HASM (NA) cells following transfection with miR-708 mimic or scrambled sequence mimic and exposure to rh-TNF-α (MT and ST, respectively, (n = 3 donors). [score:3]
The functional effect of increased miR-708 expression in these cells remains to be determined. [score:3]
Over -expression of miR-708 mimic at 50 nM and 100 nM concentrations significantly decreased CD38 transcript level (Figure  2A). [score:3]
In ASM cells, miR-708 decreased CD38 expression by decreasing phosphorylation of JNK MAPK and AKT. [score:3]
Figure 5 Effect of miR-708 transfection on ERK and p38 MAP kinase activation and expression in NA-HASM cells. [score:3]
MKP-1 expression was significantly higher in cells transfected with miR-708 mimic compared to cells transfected with the scrambled sequence mimic (Figure  6D). [score:2]
In this study, we identified miR-708 as a regulator of CD38 in HASM cells. [score:2]
A similar increase in PTEN expression was observed in AS-HASM cells following miR-708 mimic transfection compared to cells transfected with the scrambled sequence mimic (Figure  7D). [score:2]
In the current study, we found that miR-708 also regulates the phosphorylation of JNK MAP kinase in NA-HASM cells. [score:2]
Furthermore, PI3 kinase signaling is regulated by other miRNAs, including miR-708 [25]. [score:2]
Further, expression of miR-708 in AS-HASM cells was found to be higher in vehicle treated (~2-fold) and rh-TNF-α treated (>10-fold) cells when compared to NA-HASM cells (Figure  1D). [score:2]
MiR-708 directly binds to 3’UTR of CD38. [score:1]
Expression of a MAP kinase phosphatase, MKP-1, was measured by in miR-708 -transfected cells following rh-TNF-α exposure. [score:1]
To determine the activation of MAPKs and AKT following miR-708 transfection, cells were collected at 20 min or 2 h respectively after treatment with rh-TNF-α and lysed. [score:1]
To evaluate the expression of miR-708 in HASM cells obtained from non-asthmatic and asthmatic donors in the presence of rh-TNF-α, q-PCR was performed. [score:1]
Figure 7 Effect of miR-708 transfection on PTEN/AKT signaling. [score:1]
B: CD38 transcript levels following transfection with miR-708 mimic (50 nM) or scrambled sequence mimic in AS-HASM cells. [score:1]
Other miRNAs (miR-708 and miR140-3p) which showed ct values ranging from 20–30 (Figure  1A) were selected for further studies. [score:1]
Note significant attenuation of enzyme activity in cells from AS and NA after transfection with miR-708 mimic. [score:1]
A: Predicted binding sites for miR-708 and miR-140-3p in 3’UTR of CD38. [score:1]
A: NA-HASM cells were transfected with different concentrations of miR-708 mimic (mimic) or scrambled sequence mimic (scr), followed by exposure to 10 ng/ml rh-TNF-α. [score:1]
CD38 3’UTR is ~481b long and has multiple miRNA binding sites, including a site for miR-708. [score:1]
In cells transfected with miR-708 mimic, the level of phosphorylated AKT was significantly lower relative to cells transfected with the scrambled sequence mimic (Figure  7A). [score:1]
Transfection of HASM cells with miR-708 mimic had little effect on levels of phosphorylated or total ERK and p38 (Figure  5). [score:1]
A significant reduction, however, was noted in the level of phosphorylated JNK MAP kinase in growth-arrested, TNF-α exposed (20 min) cells following miR-708 transfection (Figure  6A). [score:1]
MiR-708 is known to regulate PI3K/AKT signaling and hyperproliferation of other cell types. [score:1]
Figure 4 Effect of miR-708 in combination with miR-140-3p on ADP-ribosyl cyclase activity in NA-HASM cells. [score:1]
C: Relative luciferase activity in cells co -transfected with reporter plasmid containing either wild-type (wild) or mutant (mut) CD38 3’UTR followed by transfection with 50 nM of miR-708 mimic (mimic) or scrambled sequence mimic (scr) (n = 3, experiments in triplicate). [score:1]
Figure 6 Effect of miR-708 transfection on JNK MAP kinase signaling in NA-HASM cells. [score:1]
Note significant reduction in luciferase activity following transfection with miR-708 mimic at all concentrations. [score:1]
To measure changes in the expression of CD38 [8, 20] and JNK at transcript levels (following miR-708 mimic or scrambled sequence mimic transfection), q-PCR was performed using Brilliant SYBR Green Master Mix. [score:1]
Note that no additive effect was observed in cells transfected with equimolar concentrations of miR-708 and miR-140-3p relative to miR-708 alone. [score:1]
B: Relative luciferase activity in NIH-3 T3 cells co -transfected with reporter plasmid and different concentrations of miR-708 mimic (mimic) or scrambled sequence mimic (scr) at the highest concentration (n = 3, experiments in triplicate). [score:1]
Transient transfection of primary HASM cells with miR-708 mimic, antagomir or scrambled sequence mimic at 10–100 nM was carried out in the presence of Lipofectamine® RNAiMax transfection reagent. [score:1]
Cells were transfected with 50 nM miR-708 and exposed to rh-TNF-α in the presence of actinomycin D. At time points indicated, CD38 transcript levels were quantified by q-PCR (n = 2–5 donors). [score:1]
Briefly, expression of miR-708 at constitutive levels and after induction with rh-TNF-α was measured by q-PCR after poly-adenylation. [score:1]
DMEM was from GIBCO-BRL (Grand Island, NY); rh-TNF-α was from R&D Systems (Minneapolis, MN); TRIzol, SuperScript III reverse transcriptase, NCode miRNA first-strand synthesis kit, Platinum SYBR Green quantitative PCR (qPCR) mix, Opti-MEM® reduced serum medium and Lipofectamine® RNAiMax transfection reagent were from Invitrogen Life Technologies (Carlsbad, CA); Brilliant lll Ultra-Fast SYBR Green q-PCR Master Mix from Agilent Technologies, Inc (Santa Clara CA); Fugene HD transfection reagent was from Roche Diagnostics (Indianapolis, IN); QuikChange Lightning Multi Site-Directed mutagenesis kit was from Agilent Technologies, Inc (Santa Clara, CA); control oligo (scrambled sequence mimic), miR-708 mimic (mature miR-708 sequence: 5’-AAGGAGCUUACAAUCUAGCUGGG-3’), and antagomir oligonucleotides were from Dharmacon (Lafayette, CO); Dual Luciferase Reporter Assay System was from Promega (San Luis Obispo, CA); NIH-3 T3 cells were from ATCC (#CRL-1658, Manassas, VA); chemiluminescent substrate for horseradish peroxidase (HRP) was from Millipore (Billerica, MA); rabbit primary antibodies against major MAPK family, PTEN, AKT2, AKT and β-actin as well as anti-rabbit secondary antibody were from Cell Signaling Technology (Danvers, MA); mouse primary antibodies for MKP-1, α-actin and goat-anti mouse antibodies were from Santa Cruz Biotechnology (Dallas, TX). [score:1]
In NA- and AS-ASM cells transfected with miR-708 mimic or the scrambled sequence mimic, there was comparable decay in CD38 mRNA content, with half-life ranging from 16–32 h (Figure  3D). [score:1]
D: CD38 transcript levels in NA-HASM cells following transfection with miR-708 mimic (50 nM), scrambled sequence mimic or antagomir for the miRNA (ant-mir) (n = 3 donors). [score:1]
Figure 3 Interaction of miR-708 with the 3’UTR of CD38. [score:1]
NIH-3 T3 cells seeded in 24 well plates (1.5-2.0 × 10 [5] cells/well) were co -transfected with miR-708 mimic or scrambled sequence mimic (50 nM), wild-type (or mutated) firefly Luc-CD38-3’UTR-reporter plasmid (200 ng/well) and Renilla luciferase plasmid (control) (30 ng/well), in culture medium (Opti-MEM® reduced serum medium; 100 μl), facilitated by Fugene HD transfection reagent (1 μl/well). [score:1]
MiRNAs miR-1272, miR-548, miR-208a, miR-1298, miR-708 and miR140-3p were predicted to bind to the CD38 3’UTR with high context score. [score:1]
HASM cells were transfected with miR-708 mimic or scrambled sequence mimic. [score:1]
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2
[+] score: 136
We further confirmed the miR-708 upregulation in the primary ovarian tumors upon DEX treatment (Fig 4E), which accords with our in vitro observation that miR-708 expression was upregulated by GC -mediated signaling (Fig 3A). [score:9]
We previously reported that GC -mediated signaling inhibits metastasis in ovarian cancer and specifically identified a novel regulatory mechanism of GCs in suppressing cancer metastasis by regulating a metastasis suppressor microRNA (miRNA), miR-708 [8]. [score:9]
MiR-708 expression was upregulated in the DEX -treated mice, whereas some proinflammatory cytokines as well as the number of tumor -associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment were reduced in these mice. [score:7]
MiR-708 expression in ID-8 cells significantly inhibited their migration and invasion abilities (Fig 1A and 1B), supporting our hypothesis that miR-708 plays a suppressive role in the migration and invasion of mouse-derived epithelial ovary cancer cells. [score:7]
The results revealed that miR-708 expression in ID-8 cells reduced Rap1B (Fig 1C), and this inhibition was abrogated by anti-miR-708 coexpression. [score:7]
Overall, these findings support and extend our previous results, indicating that low-dose GCs suppress ovarian cancer progression and metastasis in an immunocompetent syngeneic mouse mo del, and this suppression may not only be due to the induction of miR-708, but also the inhibition of TAMs and MDSCs at the tumor microenvironment. [score:7]
MicroRNA-708 expression inhibits mouse ovarian cancer cell Rap1B expression, migration and invasion. [score:6]
We previously demonstrated that DEX can induce miR-708, which is downregulated in the advanced stages of ovarian cancer, to inhibit the migration and invasion of human ovarian cancer cells in culture as well as the growth and metastasis of tumors derived from them in an immunocompromised xenograft mouse mo del [8]. [score:6]
Glucocorticoid suppresses cell migration and invasion by upregulating miRNA-708 transcription in ID-8 cells. [score:6]
It can induce the expression of miR-708, leading to the depletion of Rap1B and suppression of ovarian cancer metastasis. [score:5]
In agreement with our previous observation [8], we observed that GC -mediated signaling induced the expression of miR-708, leading to the depletion of Rap1B and suppression of abdominal metastasis in ovarian tumor-bearing mice with an intact immune system. [score:5]
MicroRNA-708 suppresses ovarian cancer cell migration and invasion via downregulation of Rap1B. [score:5]
We found that treatment with DEX induced the expression of miR-708, leading to the suppression of Rap1B, which resulted in the reduction of cell migration and invasion in a mouse-derived EOC cell line, ID-8 cells. [score:5]
Restoring Rap1B expression in human EOC cells abrogated miR-708 -mediated suppression of migration and invasion in cell culture and abdominal metastasis in an orthotopic mouse mo del [8]. [score:5]
Therefore, we next determined whether miR-708 regulates Rap1B expression in ID-8 cells. [score:4]
We previously reported that miR-708 suppressed cell spreading and adhesion by regulating focal adhesion formation mediated by Rap1B. [score:4]
MicroRNA-708 suppresses cell migration and invasion as well as Rap1B expression in ID-8 cells. [score:4]
This differential effect on the growth of primary tumors implies the possible involvement of immune system other than the induction of miR-708 in suppressing tumor growth and metastasis in our current immunocompetent mouse mo del. [score:3]
We further assessed whether migration and invasion abilities were mediated by GC signaling through miR-708 expression. [score:3]
Consistent with that observation, we observed that DEX treatment significantly induced miR-708 expression in ID-8 cells (Fig 3A). [score:3]
To assess whether Rap1B serves as a downstream effector of the miR-708 -mediated inhibition of ID-8 cell motility and invasiveness, we determined the role of Rap1B in cell migration and invasion. [score:3]
DEX significantly reduced both abilities of the ID-8 cells, and the depletion of the endogenous miR-708 by anti-miR-708 abrogated this DEX -mediated inhibition of cell migration and invasion (Fig 3C–3E). [score:3]
0178937.g003 Fig 3(A) miR-708 expression in ID-8 cells after 72 h of treatment with an increasing amount of DEX (100–1000nM). [score:3]
Overall, our results revealed that GCs suppress cell migration and invasion, mainly via the miR-708–Rap1B signaling pathways in ID-8 cells. [score:3]
Our previous study showed that GCs suppress ovarian cancer metastasis by inducing miR-708 in the human tumor xenograft in an immunocompromised mouse mo del [8]. [score:3]
The depletion of Rap1B by siRNA (Fig 2A) reduced both the migration and invasion abilities of ID-8 cells (Fig 2B and 2C), suggesting the key role of Rap1B in the miR-708 -mediated suppression of cell migration and invasion. [score:3]
Because GCs, such as DEX, can modulate the immune system, we wished to employ an immune competent syngeneic mouse mo del to assess the miR-708 induction and tumor inhibitory effects of DEX. [score:3]
We first examined whether miR-708 can suppress ID-8 cell migration and invasion, which were assessed using Boyden chambers transwell assays, as previously described [8]. [score:2]
GC signaling reduces the migration and invasion abilities of ID-8 cells through miR-708 induction. [score:1]
We previously reported that GCs induced miR-708 transcription in human ovarian cancer cells [8]. [score:1]
The precursor miR-708 was purchased from Applied Biosystems (Carlsbad, CA), and anti-miR-708 was obtained from GeneDireX (Vegas, NV). [score:1]
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3
[+] score: 56
Reduced expression of hsa-miR-708 expression has also been seen in blood taken from old individuals in comparison to young individuals 39. [score:5]
In conclusion, we present evidence that three miRNAs, miR-203-3p, miR-664-3p and miR-708-5p are robustly associated with median strain lifespan in 6 well-characterized inbred strains of mice, and that both early life (miR-203-3p) and later life (miR-664-3p and miR-708-5p) changes in their expression may modulate the expression of target genes in several very well-known aging and longevity pathways. [score:5]
279 miRNAs were found to be expressed above the limit of detection and of these, 5 (miR-297b-5p, miR-708-5p, miR-224-5p, miR-203-3p and miR-327) were shown to be differentially expressed between average-lived and long-lived strains after correction for multiple testing (significance cutoff: p < 0.0002). [score:5]
Also predicted to be enriched for miR-203-3p, miR-664-3p and miR-708-5p binding sites are the ‘Pathways in cancer (mmu05200)’ pathway, the ‘MAPK signalling pathway (mmu04010), the ‘signalling pathways regulating pluripotency of stem cells (mmu04550)’ pathway and the ‘TGF-beta signalling pathway (mmu04350)’, with 33, 26, 14 and 10 genes targeted respectively (FDR-adjusted p-values = 0.03, 0.005, 0.05 and 0.0001 respectively). [score:4]
The lifespan effects of miR-203-3p, miR-664-3p and miR-708-5p are probably mediated by altered regulation of their target genes. [score:4]
This may be partially explained if the effects on miR-708-5p expression reflect a balance between protection from malignancy and maintained proliferative capacity. [score:3]
Analysis of expression in relation to age of the animals revealed that miR-203-3p was not significantly associated with age whereas both miR664-3p and miR-708-5p were positively associated (see Supplementary Table S4). [score:3]
Gene set enrichment analysis using the DIANA miRPath webtool 21 reveals 15 pathways that are enriched for miR-203-3p, miR-664-3p and miR-708-5p target genes. [score:3]
We identified 15 pathways that were predicted to be enriched in miR-203-3p, miR-664-3p or miR-708-5p target genes, many of which are known to be associated with aging or longevity (see Table 2). [score:3]
for miR-708-5p showed no significant difference in expression between young and old animals of average lifespan (β-coefficient = 0.12; p = 0.33, see Supplementary Table S5 and Fig. 2). [score:3]
In our data, elevated, rather than decreased miR-708-5p expression was found to be associated with longer lifespan. [score:3]
MicroRNA miR-708-5p also showed increased expression in strains of longer lifespan in the combined analysis of old and young animals, after correction for multiple testing (β-coefficient = 0.50; p = 1.61 × 10 [−6], see Supplementary Table S2 and Fig. 1g). [score:3]
Prominent pathways targeted by all 3 miRNAs include the ‘FoxO signalling pathway (mmu04068)’ and ‘mTOR signalling pathway (mmu04150)’, which contain 16 and 11 genes with predicted miR-203-3p, miR-664-3p and miR-708-5p binding sites (FDR-adjusted p-values = 0.02 and 0.01 respectively). [score:3]
Again, the changes we noted were most evident in the old animals of the long-lived strains, suggesting that increased expression of miR-708-5p may also be a later life effect on longevity. [score:3]
The observation that many of the pathways implicated contain genes that are known to control shared outcomes such as apoptosis, cell cycle regulation, differentiation, proliferation, cell survival, autophagy and DNA repair adds strength to the hypothesis that miR-203-3p, miR-664-3p and miR-708-5p may have functionality in terms of longevity. [score:2]
How to cite this article: Lee, B. P. et al. MicroRNAs miR-203-3p, miR-664-3p and miR-708-5p are associated with median strain lifespan in mice. [score:1]
Here we show that three miRNAs; miR-203-3p, miR-664-3p and miR-708-5p, are significantly associated with strain lifespan in mouse spleen. [score:1]
We found that 3 miRNAs; miR-203-3p, miR-664-3p and miR-708-5p were associated with median strain lifespan (Supplementary Table S2). [score:1]
MicroRNA miR-708-5p was also positively correlated with longer lifespan. [score:1]
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4
[+] score: 52
Of these, 12 (mir-9, mir-200c, mir-708, mir-377, mir-26b, mir-296, mir-369, mir-32, mir-1965, mir-1190, mir-135b and mir-201) were differentially up-regulated and five (mir-291a, mir-190b, mir-297c, mir-713 and mir-470) were differentially down-regulated. [score:7]
Among them, miR-135b and miR-708 displayed a significant up-regulation in primary hippocampal neurons with H [2]O [2] stimulation for 6 h. The regulation of miRNA on its target genes is a rapid process, and the oxidative stress plays an important role in the onset of neurodegenerative disorders. [score:7]
The up-regulated miRNAs, including miR-708, miR-296, miR-200c, miR-377 and miR-1190, were all strongly predicted to affect target genes involved in the MAPK pathway. [score:6]
Analysis of miR-708 targets showed that miR-708 mainly took part in the positive regulation of small GTPase -mediated signal transduction, protein amino acid phosphorylation, positive regulation of cell proliferation, neuron development, etc. [score:6]
Given that miR-708 is upregulated in mouse hippocampal neurons induced by oxidative stress, it is, therefore, likely that aberrant expression of miR-708, at least in part, contributes to the pathology of AD. [score:6]
Mitogen-activated protein kinase (MAPK) signaling pathway was one of the most significant pathways to be affected by 74 target genes of miR-708, miR-296, miR-200c, miR-377 and miR-1190 (Table 1). [score:3]
Bioinformatic analysis of miR-708 target genes showed that five genes (Map3k13, Kras, Rap1b, Nras and Csf1) were predicted to affect the MAPK signaling pathway. [score:3]
To further illuminate the possible roles of miR-135b and miR-708 in the pathogenesis of AD, Gene Ontology (GO) enrichment for biological processes and molecular functions of miR-135 and miR-708 targets were performed. [score:3]
Functional Analysis of Targets of miR-135b and miR-708. [score:3]
The Enrichment for Gene Ontology (GO) term of miR-708 targets revealed that miR-708 mainly took part in the process of cell apoptosis, which might explain the results of TUNEL and PI staining. [score:3]
It was showed that miR-135b (p < 0.01) and miR-708 (p < 0.05) expressed at higher levels in H [2]O [2] -treated primary hippocampal neurons compared with control cells, consistent with the results of microarray (Figure 4). [score:2]
Based on the relevance to neurodegenerative disorders, their expression levels (total counts in hippocampus) and the possible functions predicted by KEGG considered [25], we chose five miRNAs, including miR-32, miR-196b, miR-26b, miR-708 and miR-135b, to validate microarray results among 17 miRNAs. [score:2]
The miRNA participated pathway analysis involving miR-708 has been previously studied in other reports about lung cancer [28], childhood acute lymphoblastic leukemia [29] and renal cancer [30]. [score:1]
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5
[+] score: 27
Other miRNAs from this paper: hsa-mir-708
We found no difference between all four groups of animals when analyzed by one-way Anova suggesting that in ADRP retina: 1) the CHOP ablation does not promote modulation of the miR-708 expression (T17M RHO CHOP+/+ vs T17M RHO CHOP−/−) as it has been proposed for the MEFs treated with thapsigardin [15] and 2) the ER stress (T17M RHO) down-regulates the level of miR-708 in the CHOP deficient retina (CHOP−/− vs T17M RHO CHOP−/−). [score:6]
In that study, it was shown that CHOP protein controls the expression of rhodopsin during ER stress through miR-708 in the first intron of Odz4, a target of the UPR transcription factor CHOP. [score:5]
We also learned that the CHOP gene controls the expression of RHO mRNA during ER stress through transcriptional regulation of miR-708, which is known to be increased under induced UPR [15]. [score:4]
Figure S3 Ablation of the CHOP protein in ADRP retina does not modulate the miR-708 expression. [score:3]
It also points the fact that the additional regulatory pathways besides the transcriptional regulation of the RHO by miR-708 could be responsible for accelerated retinal degeneration of T17M RHO CHOP−/− mice. [score:3]
That study revealed that this control occurs through transcriptional regulation of miR-708 by CHOP protein and assigned the CHOP protein a cytoprotective function. [score:2]
However, T-test comparison revealed that there is a statistically significant difference between CHOP−/− and T17M RHO CHOP−/− mice suggesting that the ER stress promotes reduction of miR-708 in CHOP deficient retinas. [score:1]
Next, we attempted to understand the cause of modulation of the RHO mRNA and performed the experiment in which we analyzed the level of miR-708 (Fig. S3). [score:1]
Therefore, we performed experiment in which we analyzed the level of miR-708 in ADRP retina. [score:1]
Overall, the conclusion we made supports the general finding presented by Behram et al. [15] that the combination of ER stress and CHOP ablation promotes reduction of the miR-708 (wild-type vs T17M RHO CHOP−/−, P = 0.03). [score:1]
[1 to 20 of 10 sentences]
6
[+] score: 18
We focused on the 4 miRNAs that were differentially expressed in early stage lesions of both genetic and inflammatory origin (miR-215, miR-31, miR-708, miR-135b). [score:3]
Eight high priority miRNAs were identified: miR-215, miR-137, miR-708, miR-31, and miR-135b were differentially expressed in APC tumors and miR-215, miR-133a, miR-467d, miR-218, miR-708, miR-31, and miR-135b in colitis -associated tumors. [score:3]
Differential expression of miR-708 and miR-218 was not reported in the literature. [score:3]
This curation step reduced the number of high probability differentially expressed miRNAs in APC tumors to 5 and the number of such miRNAs in CAC tumors to 7. As shown in Table 1, two miRNAs were repressed in APC tumors (miR-215 and miR-137), compared to adjacent control epithelium, whereas 3 miRNAs were induced (miR-708, miR-31, miR-135b). [score:2]
Four of these (miR-215, miR-708, miR-31, and miR-135b) were common to both tumors types, and dysregulation of these miRNAs was confirmed in an independent sample set. [score:2]
Three miRNAs were induced in both APC and CAC samples (miR-31, miR-135b, and miR-708) and 1 miRNA was repressed in both APC and CAC samples (miR-215). [score:1]
Summary of top GO functions identified for miR-215, miR-31, miR-135b, and miR-708 by Ingenuity Pathway Analysis. [score:1]
We also note that currently there is no report of miR-708 in human colon cancers, in contrast to our data which indicates that this miRNA is dramatically induced in mouse colonic tumors. [score:1]
Nevertheless, we were able to validate our four most prominent miRNAs (miR-215, miR-708, miR-135b, miR-31) in an independent set of APC and CAC tumors. [score:1]
As shown in Figure 4, repression of miR-215 was confirmed in both CAC and APC tumor samples, whereas induction of miR-708, miR-31, and miR-135b was likewise confirmed in tumors of both origins. [score:1]
[1 to 20 of 10 sentences]
7
[+] score: 10
The fact that 3 tumor-suppressive miRNAs, i. e., miR-34a [9], miR-708 [28], and miR-199a-3p (this study), simultaneously target 5 different sites at the CD44 3′-UTR (Figure 6A), highlights the critical importance of CD44 in regulating CSC properties [6– 10]. [score:6]
Furthermore, another miRNA, miR-708, was also reported to negatively regulate PCSC activity by targeting CD44 at two different sites [28](Figure 6A). [score:4]
[1 to 20 of 2 sentences]
8
[+] score: 9
23 Mediates tumor-suppressive epigenetic activities of vitamin D miR-632 5.15/5.80 2.50/1.45 6.04/5.06 4.63/4.77 3.34/13.63 5.92/5.30 Downregulation of DNAJB6 (HSP40 family); Implicated in invasive activity of breast cancer cells miR-664b-5p 5.26/1.82 1.24/0.53 1.36/1.99 3.49/3.83 7.41/1.79 2.52/4.02 Decreases MAPK-1 expression which reduces TNF-α miR-708-3p 0.74/0.41 0.81/4.93 0.47/0.58 0.69/2. [score:8]
Likewise, in naproxen -treated mice exposed to MCS modulation of 3 miRNAs in both lung and blood serum (miR-181b, miR-344d, and miR-708) correlated with protection against pulmonary microadenomas, while one miRNA only (miR-711), correlated with protection against pulmonary adenomas, was modulated in both body compartments. [score:1]
[1 to 20 of 2 sentences]
9
[+] score: 7
Meanwhile, mmu-miR-708 and mmu-miR-879 were significantly upregulated (fold change ≥ 2 and p value < 0.05) (Table 1, Figure 3). [score:4]
The six miRNAs, including mmu-miR-615, mmu-miR-124, mmu-miR-376b, mmu-let-7e, mmu-miR-708, and mmu-miR-879 had a total of 349 validated target genes in the miRWalk database (Table 2). [score:3]
[1 to 20 of 2 sentences]
10
[+] score: 7
Other miRNAs from this paper: hsa-mir-708
Although typically associated with an upregulation of apoptotic pathways, CHOP has also been found to play a protective role to improve protein-folding capacity and cell survival by transcriptional regulation of particular target genes and microRNAs such as GADD34 (26) and miR-708 (45). [score:7]
[1 to 20 of 1 sentences]
11
[+] score: 7
Among them, seven miRNAs including three that were down-regulated (mmu-miR-708-5p, mmu-miR-92a-2-5p, and mmu-miR-711) and four that were up-regulated (mmu-miR-714, mmu-miR-134-5p, mmu-let-7a-2-3p, and mmu-miR-27a-5p) were predicted to be involved in cellular response to stimulus. [score:7]
[1 to 20 of 1 sentences]
12
[+] score: 6
74, 75, 76 The tumour suppressive miR-708 and miR-126 on the other hand are upregulated during reprogramming in p53 wt cells and reduced in p53R172H cells. [score:6]
[1 to 20 of 1 sentences]
13
[+] score: 4
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, hsa-mir-708, hsa-mir-301b, 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 down-regulated miRNAs, 24 miRNAs showed a >5-fold decrease, including four miRNAs, i. e. miR-205, miR-503, miR-708 and miR-2115*, which were undetectable in the metastatic line. [score:4]
[1 to 20 of 1 sentences]
14
[+] score: 4
These searches identified 8 miRNAs (miR-7a, miR-7b, miR-28, miR-186, miR-381, miR-876, miR-543, and miR-708) that might target CRX. [score:3]
control miR-7b mimcs CRX 1.005 ± 0.090.43 ± 0.04 [*] miR-7b 1.00 ± 0.042.62 ± 0.16 [*] Con miR-186 mimics CRX 1.05 ± 0.14 1.07 ± 0.09 miR-186 1.00 ± 0.021.25 ± 0.02 [*] Con miR-7a mimics CRX 1.02 ± 0.08 0.91 ± 0.016 miR-7a 1.01 ± 0.15 1.15 ± 0.06 Con miR-876 mimics CRX 1.00 ± 0.04 1.14 ± 0.05 miR-876 1.00 ± 0.09 1.25 ± 0. 14 Con miR-708 mimics CRX 1.00 ± 0.11 1.02 ± 0.10 miR-708 1.00 ± 0.03 0.89 ± 0.07 Con miR-381 mimics CRX 1.01 ± 0.10 1.25 ± 0.15 miR-381 1.00 ± 0.01 0.83 ± 0.09 Con miR-543 mimics CRX 1.00 ± 0.060.39 ± 0.02 [*] miR-543 1.09 ± 0.142.56 ± 0.18 [*] Con miR-28 mimics CRX 1.00 ± 0.040.36 ± 0.02 [*] miR-28 1.00 ± 0.092.08 ± 0. 10 [*] * P < 0.05. [score:1]
[1 to 20 of 2 sentences]
15
[+] score: 4
Such included some of the most upregulated miRNA in the array data, such as miR-379, miR-671-5p and miR-708 (Figure S4). [score:4]
[1 to 20 of 1 sentences]
16
[+] score: 4
Other miRNAs from this paper: mmu-mir-31, mmu-mir-489
The function of mir-708 is also unknown, but the gene expression mechanism of Odz4 might be important for efficient skeletal muscle regeneration. [score:3]
Like calcitonin receptor genes, the Odz4 intron contains a quiescent satellite cell-specific microRNA, mir-708 (Cheung et al., 2012). [score:1]
[1 to 20 of 2 sentences]
17
[+] score: 4
Since Chop has been shown to regulate the expression of rhodopsin through a microRNA, miR-708, in 293T cells [45], deleting Chop could alter rhodopsin levels in photoreceptors and potentially influence retinal degeneration. [score:4]
[1 to 20 of 1 sentences]
18
[+] score: 4
Other miRNAs from this paper: mmu-mir-30c-2, mmu-mir-211, mmu-mir-455
For example, miR-708, which is transcribed from an intron of a CHOP-regulated gene, Odz4, controls the expression of rhodopsin in retina and prevents it from entering the ER [7]. [score:4]
[1 to 20 of 1 sentences]
19
[+] score: 3
Lee JW miR-708-3p mediates metastasis and chemoresistance through inhibition of epithelial-to-mesenchymal transition in breast cancerCancer Sci. [score:3]
[1 to 20 of 1 sentences]
20
[+] 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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
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21
[+] score: 3
Fold changes for miR-708-5p, miR-30a-5p and miR-221-3p with qPCR were in the opposite direction than that of small RNA sequencing. [score:2]
The miRNAs we tested were let-7a-5p, miR-30a-5p, miR-30c-2-3p, miR- 99b-5p, miR-143-3p, miR-199a-3p, miR-221-3p, miR-222-3p, miR-455-3p, and miR-708-5p. [score:1]
[1 to 20 of 2 sentences]
22
[+] score: 3
The miR-26a, miR-28a or miR-708 was coexpressed with the GSK3 β 3′-UTR reporter, respectively, in a neuronal cell line CAD, which allowed high-efficiency transfection. [score:3]
[1 to 20 of 1 sentences]
23
[+] score: 2
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-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-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-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, 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
88E-0327mmu-miR-451mir-4510.3310.722.79E-046.57E-0366mmu-miR-669c-5pmir-4670.178.847.68E-037.41E-0255mmu-miR-485-3pmir-4850.196.755.52E-036.39E-0265mmu-miR-669nmir-669n0.147.887.46E-037.31E-0260mmu-miR-674-5pmir-6740.178.646.08E-036.45E-0254mmu-miR-676-3pmir-6760.156.634.48E-035.28E-0211mmu-miR-7a-5pmir-70.249.171.37E-057.91E-0436mmu-miR-708-5pmir-7080.179.389.09E-041. [score:1]
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[+] score: 1
This shows that they are preferentially edited by ADAR2 (miR-467c at position 3, miR-467e at position 4, miR-708* at position 21 and miR-411 at position 2) (see Table 4). [score:1]
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[+] score: 1
There are a few miRNA, such as miR-320 [20], miR-666 and miR-708 [21], which have identified as potential modulator of AQP1. [score:1]
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[+] score: 1
Our previous study found that miR-196a, miR-486-5p, miR-664-star, and miR-378-star were significantly increased whereas miR-10a, miR-708, and miR-3197 were decreased in old hBM-MSCs. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-708
MET potentiated rapamycin and cisplatin effects on gastric cancer in mice [23] and induced ER stress -dependent apoptosis through miR-708-5p/NNAT pathway in prostate cancer [24]. [score:1]
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