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28 publications mentioning hsa-mir-329-1

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-329-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 380
Consistent with above mentioned results, miR-329 is found to significantly decrease the phosphorylation levels of intracellular kinases Akt, and upregulate the expression of p 21 in miR-329 -overexpressing cells, while p Akt phosphorylation was increased and the expression of p 21was inhibited in the miR-329 -inhibited cells. [score:14]
The important downstream targets of Akt in the regulation at G1/S transition, cyclin D1 and p21 were respectively downregulated and upregulated in miR-329 -overexpressing cells. [score:12]
MiR-329 significantly decreased the phosphorylation levels of intracellular kinases Akt and expression of cyclin D1, but the expression of p 21 was upregulated, cell growth was suppressed by inhibiting E2F1 -mediated Akt pathway. [score:11]
Strikingly, we found that enforced expression of miR-329 in LN18 and T98G glioma cells drastically inhibited their anchorage-independent growth ability (Figure  2C), as shown by decreased colony numbers and sizes, these results suggested that miR-329 upregulation inhibits glioma cell tumorigenicity in vitro. [score:10]
Our results showed that the expression of E2F1 was regulated by miR-329 and the level of E2F1 protein expression was inversely correlated with miR-329 expression in glioma cells. [score:8]
Furthermore, ectopic expression of miR-329 inhibited the cell proliferation and anchorage-independent growth of glioma, while miR-329 inhibition had the opposite effect, this point was further confirmed in 1: Figure S1. [score:7]
We constructed cell mo dels of over -expressing miR-329 and down -expressing miR-329 in glioma cells and screened expressing levels of miR-329 and E2F1 in a group of glioma cells. [score:7]
As shown in Figure  4C, overexpressing miR-329 only decreased expression of a GFP vector containing the E2F1 3′UTR, but had no effect on GFP-γ-tubulin expression, the result suggested that miR-329 specifically affected the 3′UTR of E2F1. [score:7]
Furthermore, we also examined whether the Akt inhibitor can synergize with miR-329 in inhibiting proliferation in glioma cells, the levels of Akt phosphorylation are decreased by treatment with Akt inhibitor IV, in which the p 21 is significantly increased and cyclin D1 is decreased. [score:7]
Importantly, western blotting analysis showed that ectopic expression of miR-329 dramatically decreased, but inhibition of miR-329 increased E2F1 protein expression in both LN18 and T98G glioma cells (Figure  4B). [score:7]
Interestingly, the protein level of cyclin D1, a CDK regulator important for regulating the G1/S transition, was downregulated in LN18 and T98G glioma cells transfected with miR-329 mimic, but increased in the cells transfected with miR-329 inhibitor, compared with control cells (Figure  4B). [score:7]
Qur analysis revealed that restoring miR-329 expression attenuated protein level of E2F1 by posttranscription regulation, and inhibited cell cycle progression in glioma. [score:6]
The miRNA expressing profile of glioma samples and cell lines suggested that miR-329 is one of down-regulated miRNAs [11]. [score:6]
In this study, we showed that miR-329 can significantly decrease the phosphorylation of Akt, miR-329 might achieve anti-proliferation and induce G1/S transition through negatively regulating E2F1 expression and inhibiting Akt pathway at least in part. [score:6]
Restoring miR-329 expression attenuated protein level of E2F1 by posttranscription regulation, E2F1 gene was identified as the target of miR-329. [score:6]
To examine whether miR-329 downregulation of E2F1 was mediated by the 3′-untranslated region (3′UTR) of E2F1, we subcloned the E2F1 3′UTR fragment, containing the miR-329 binding site, into pEGFP-C1 and pGL3 dual luciferase reporter vectors. [score:6]
Figure 2 Upregulation of miR-329 inhibits the cell proliferation in glioma. [score:6]
E2F1 was identified as a significant target of miR-329 by luciferase assays, miR-329 was able to induce the G1/S arrest and inhibit proliferation of glioma cells through E2F1 -mediated suppression of Akt pathway. [score:6]
The overexpression of miR-329 also efficiently reduced the expression of the luciferase reporter in the pGL3–E2F1-3′UTR group but did not have the effect in the pGL3–E2F1-3′UTR-mut group (Figure  4E). [score:5]
As shown in Figure  1B, miR-329 expression levels of all cell lines were lower than that of NHA, while expression levels of E2F1 in the cell lines were higher (Figure  1C). [score:5]
The pBABE-E2F1 overexpressing E2F1and pBABE-E2F1-3′UTR were respectively transfected into glioma cells with miR-329 mimic expressing using the Lipofectamine 2000 reagent. [score:5]
As shown in Figure  1B, miR-329 expression levels of SNB19 cell lines were lower than that of other cell lines while expression levels of it in the U251 cell lines were higher than that of other cell lines. [score:5]
Our results showed that miR-329 significantly decrease the expression level of intracellular p-Akt and E2F1 in miR-329 -overexpressing cells. [score:5]
A ) MTT assays revealed that upregulation of miR-329 inhibited cell growth of glioma cell lines of T98G and LN18. [score:5]
Overexpression of miR-329 blocked G1/S transition in LN18 and T98G cell lines, dramatically suppressed cell proliferation and the ability of colony formation. [score:5]
The average miR-329 expression was normalized by U6 expression. [score:5]
The key finding of the current study is that miR-329 expression was markedly downregulated in glioma cells and glioma tissues, compared with that in nonneoplastic brain specimens and primary normal human astrocytes (NHA). [score:5]
To explore the role of miR-329 downregulation in the development and progression of glioma, we examined its effect on cell proliferation. [score:5]
B ) Western blotting analysis of E2F1,pAkt, Akt, p21, cyclinD1 expression in cells transfected with miR-329 or the miR-329 inhibitor, β-actin served as the loading control. [score:5]
The result of colony formation assay showed overexpressing E2F1 significantly increased the proliferation rate of LN18 and T98G glioma cells compared with that cells expressing E2F1-3′UTR (Figure  5A), the rescuing experiment further confirmed that the inhibitory role of miR-329 in glioma cells may be mediated by E2F1. [score:5]
MicroRNAs have recently emerged as key regulators of cancers, miR-329 located on 14q32.31 is one of down-regulated miRNAs in glioma, but the function and molecular mechanisms of miR-329 in determining the malignant phenotype of human glioma are elusive. [score:5]
C ) Upregulation of miR-329 inhibited glioma cell tumorigenicity as determined by the anchorage-independent growth assay. [score:5]
Targeting to the miR-329/E2F1 interaction or rescuing miR-329 -expression may be a new therapeutic application to treat glioma patients in the future. [score:5]
We also showed that miR-329 inhibits proliferation through E2F1 -mediated suppression of Akt phosphorylation in glioma cells. [score:5]
MiR-329 may inhibit cell proliferation in human glioma cells through regulating E2F1 -mediated suppression of Akt pathway. [score:5]
Analysis with the use of two publicly available algorithms (TargetScan and miRanda), we found that E2F1 mRNA is theoretically the target gene of miR-329 (Figure  4A). [score:5]
This is the first study to show that the oncogene E2F1 is negatively regulated by miR-329 at the posttranscriptional level through a specific target site (nt 1655–1661) within the 3′-UTR. [score:4]
These results suggested that the proliferative effect of inhibiting miR-329 in glioma cells may occur through regulation of G1/S transition. [score:4]
These results provided further evidence that miR-329 may negatively regulate the Akt survival pathway through E2F1 -mediated suppression of Akt phosphorylation and play an important role in cell proliferation of glioma. [score:4]
Figure 5 MiR-329 inhibits cell proliferation through targeting E2F1 3′UTR in glioma. [score:4]
Downregulation of miR-329 in glioma. [score:4]
Figure 4 MiR-329 suppresses E2F1 expression and Akt pathway. [score:4]
A MTT assay showed that miR-329 upregulation significantly inhibited the proliferation rate of LN18 and T98G glioma cells (Figure  2A), and this was further confirmed by a colony formation assay (Figure  2B). [score:4]
Figure 3 Inhibition of miR-329 promotes cell proliferation in glioma. [score:3]
Downregulation of miR-329 was also found in clinical samples compared with nonneoplastic brain specimens (Figure  1A). [score:3]
Collectively, our results suggest that miR-329 may induce the G1/S arrest and inhibit cell proliferation of glioma. [score:3]
Furthermore, we found that transfection of the miR-329 inhibitor drastically increased the percentage of cells in the S peak but decreased the percentage of cells in the G0/G1 peak (Figures  3D and 3E). [score:3]
Therefore, miR-329 might be a potential therapeutic target for glioma that requires more in-depth analysis. [score:3]
D ) Representative micrographs (left) and quantification of BrdU incorporating-cells after transfection with miR-329 inhibitor or NC. [score:3]
Similarly, the result of flow cytometry showed that miR-329 overexpression decreased the percentage of cells in S phase and significantly increased the percentage of cells in G1/G0 (Figure  2E). [score:3]
We further examined the effect of miR-329 inhibition on cell proliferation in glioma. [score:3]
The vectors pBABE-E2F1 overexpressing E2F1 and pBABE-E2F1-3′UTR including miR-329 3′UTR binding site were constructed. [score:3]
MiR-329 directly targets E2F1 in glioma cells. [score:3]
The anti-proliferation effect of miR-329 partly is related with the inhibition of Akt pathway mediated E2F1. [score:3]
E ) Flow cytometric analysis of the indicated glioma cells transfected with NC or miR-329 inhibitor. [score:3]
Cells (4×10 [4]) were seeded in triplicates in 24-well plates and allowed to settle for 24 h. The miR-329 mimics, the miR-329-mut, and anti-miR-329 inhibitor purchased from RiboBio (RiboBio Co. [score:3]
Overexpression of miR-329 in SNB19 cells inhibited the proliferation ability of cells and the proliferating cells were significantly decreased, this was confirmed by colony formation assay and BrdU incorporation assay (Additional file 1: Figure S1C, S1D, S1E). [score:3]
Collectively, these results demonstrate that E2F1 is a bona fide target of miR-329. [score:3]
A ) Predicted miR-329 target sequence (blue) in the 3′UTR of E2F1 (E2F1-3′UTR) and positions of the mutated nucleotides (green) in the miR-329 (miR-329 mut). [score:3]
So miR-329 may act as the role of tumor suppressor in glioma cells. [score:3]
The E2F1 was identified as the target of miR-329. [score:3]
C ) Inhibition of miR-329 increased the anchorage-independent growth of glioma cells. [score:3]
E) Quantification of BrdU incorporating-cells after transfection with miR-329, miR-329 inhibitor or NC. [score:3]
Nine patients with GBM were analyzed for the expression of miR-329 by quantitative RT–PCR. [score:3]
MiR-329 expression of each cell line was compared to the average expression level of primary normal human astrocytes (NHA). [score:3]
A ) Real-time PCR analysis of miR-329 expression in three nonneoplastic brain specimens and primary glioma tissues of nine individual patients. [score:3]
Inhibition of the miR-329 expression in U251 increased the proliferation ability of cells and the proliferating cells were significantly increased, this was shown in colony formation assay and BrdU incorporation assay (Additional file 1: Figure S1C, S1D, S1E). [score:3]
First, we examined miR-329 expression in GBM cell lines. [score:3]
In addition, the anchorage-independent growth ability of LN18 and T98G glioma cells was significantly increased in response to miR-329 inhibitor (Figure  3C). [score:3]
B ) Real-time PCR analysis of miR-329 expression in primary normal human astrocytes (NHA) and glioma cell lines (including A172, LN340, U118MG, LN464, SNB19, LN18, T98G, and U251MG). [score:3]
Figure 1 Expression analysis of miR-329 in glioma cell lines and glioma tissues. [score:3]
The regulation of miR-329 on Akt pathway was determined by western blot. [score:2]
MiR-329 might suppress the ability of colony formation and induce G1/S transition in glioma cells. [score:2]
D ) Luciferase reporter assay of the indicated cells transfected with the pGL3-E2F1-3′UTR reporter and increasing amounts (10, 50 nM) of miR-329 mimic, miR-329 inhibitor or miR-329 mut oligonucleotides. [score:2]
MiR-329 inhibition increases cell proliferation in glioma. [score:2]
A ) MTT assays revealed that inhibition of miR-329 increased cell growth of glioma cell lines of T98G and LN18. [score:2]
MiR-329 inhibits cell proliferation in SNB19 and U251 glioma cells. [score:2]
Click here for file MiR-329 inhibites cell proliferation in SNB19 and U251 glioma cells. [score:2]
1: Figure S1 MiR-329 inhibites cell proliferation in SNB19 and U251 glioma cells. [score:2]
MiR-329 overexpression reduces cell proliferation in glioma. [score:2]
To validate that miR-329 can directly bind to and regulate the levels of E2F1 mRNA through the predicted binding sites, a mutant version of the reporter (pGL3–E2F1-3′UTR-mut plasmids) and altering bases in the putative miR-329 binding sites (miR-329 mut) were used in luciferase reporter assay. [score:2]
The consistent and dose -dependent reduction of luciferase activity was observed following miR-329 transfection in both glioma cells, the reporter assay revealed that the repressive effect of miR-329 on the luciferase activity of E2F1 3′UTR was abolished by miR-329 inhibitor but did not have the effect in the miR-329 mut group (Figure  4D). [score:2]
In this study, we aimed to determine the role of miR-329 in determining the proliferation of glioma cells and study the regulatory mechanism of miR-329 in glioma cells. [score:2]
MiR-329 inhibites the Akt pathway. [score:2]
The target of miR-329 was determined by luciferase assays. [score:2]
Our results suggested that anti-proliferation of miR-329 may be related with theharrest of G1/S in glioma cells. [score:1]
Consistent with above mentioned results, MTT and colony formation assays showed that miR-329 suppression dramatically increased the growth rate of both LN18 and T98G glioma cells as compared with that of control cells transfected with negative control (NC) (Figures  3A and 3B). [score:1]
D ) Representative micrographs (left) and quantification of BrdU incorporating-cells after transfection with miR-329 or NC. [score:1]
E ) Flow cytometric analysis of the indicated glioma cells transfected with NC or miR-329. [score:1]
The plasmid was sequenced and named pcDNA6.2-GW/EmGFP/ miR-329 (pre-miR-329). [score:1]
Using a BrdU incorporation assay, we found that the percentage of cells in S phase was dramatically decreased in miR-329 -overexpressing LN18 (12.25%) and T98G (13.43%) cells compared with control cells (LN18 cells, 27.25%; T98G cells, 28.43%; Figure  2D). [score:1]
We have examined the role of miR-329 in biological behaviors of human glioma cells and its molecular mechanism. [score:1]
However, the biological function of miR-329 in glioma was not be fully elucidated, the role of it in protection against apoptosis and in cell survival was still worth further studying. [score:1]
The candidate pre-miRNA-329 of double-stranded oligonucleotides was generated for cloning into the pcDNA6.2-GW/ EmGFP vector (Invitrogen, Carlsbad, CA, USA). [score:1]
The effects of miR-329 on cell cycle were studied by flow cytometry. [score:1]
However, the function and molecular mechanism of miR-329 in determining the malignant phenotype of human glioma are elusive. [score:1]
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2
[+] score: 161
Herein we report for the first time that TLR2 activation by PDG induces miR-329 expression, which plays a pivotal role in regulating PDG -induced trophoblast apoptosis and inhibition of IL-6 expression by targeting the NF-κB subunit, p65. [score:10]
Furthermore, a specific miR-329 inhibitor prevented PDG -mediated inhibition of NF-κB p65 and IL-6 mRNA expression, and inhibited PDG -induced apoptosis in the TLR6 [-] trophoblast cells. [score:9]
Since PDG upregulated trophoblast miR-329, which is predicted to target NF-κB p65, we hypothesized that miR-329 through this mechanism, might be regulating TLR2 -mediated apoptosis and IL-6 mRNA expression. [score:9]
miR-329 regulates PDG -induced trophoblast apoptosis and inhibition of IL-6 expression by targeting NF-κB p65. [score:8]
Treatment of scramble control cells with PDG significantly reduced NF-κB p65 and IL-6 mRNA expression levels and upregulated caspase-3 activity, and these responses were significantly reversed by the presence of the anti-miR-329 inhibitor. [score:8]
Our findings suggest that miR-329 plays a pivotal role in regulating human first trimester trophoblast cell responses to PDG by targeting the NF-κB p65 subunit, leading to apoptosis and inhibition of IL-6 expression, and TLR6 reverses this cellular response by preventing the TLR2 -mediated induction of miR-329. [score:8]
PDG treatment significantly upregulated trophoblast miR-329, miR-23a, miR-let-7c, and miR-23b expression in TLR6 [-], and this was significantly inhibited by the presence of TLR6 (TLR6 [+]). [score:8]
In this current study we have identified miR-329 as playing a pivotal role in mediating PDG -induced trophoblast apoptosis and inhibition of IL-6 expression by targeting the NF-κB subunit, p65. [score:7]
In addition to miR-329, we have identified 2 miRs, miR-23a and let-7c, that appear to regulate trophoblast IL-6 expression by directly targeting its mRNA. [score:7]
After identifying miR-329 a potential regulator of NF-κB p65 mRNA expression, we next considered the possibility of the involvement of other miRs that can regulate IL-6 by directly targeting its mRNA. [score:7]
Having identified miR-329 as a regulator of trophoblast IL-6 expression through the NF-κB p65 pathway, we also considered the involvement of additional miRs that might regulate the PDG -mediated IL-6 response by directly targeting IL-6 mRNA. [score:7]
Following treatment with PDG, miR-329 expression was upregulated in TLR6 [-] cells and this was completely prevented in the presence of TLR6. [score:6]
However, as shown in Figure 4A, PDG treatment significantly increased the expression of miR-329 in TLR6 [-] cells by 1.73 ± 0.42 fold, while miR-329 expression was unchanged in PDG -treated TLR6 [+] cells. [score:5]
We believe this study to be the first report that TLR2 activation by PDG induces miR-329 expression, and that miR-329 appears to target NF-κB p65 mRNA. [score:5]
However, low expression levels of miR-329 correlate with survival in glioblastoma multiforme patients [47], studies of hippocampal neurons suggest it to be involved in dendritic outgrowth [48], and miR-329 expression is decreased in airway smooth muscle treated with IL-1β, TNFα, and IFNγ [49]. [score:5]
In contrast, PDG treatment of the cells transfected with the anti-miR-329 inhibitor had no effect on NF-κB p65 expression (Figure 5B). [score:5]
The anti-miR-329 inhibitor significantly reduced miR-329 expression when compared to the scramble control sequence (data not shown). [score:4]
As shown in Table 1, PDG-treatment increased miR-329 expression by 1.85 fold in TLR6 [-] cells, while there was a 0.88 fold change in miR-329 expression in PDG -treated TLR6 [+] cells when compared to the NT controls. [score:4]
Through a global microRNA microarray, bioinformatics databases, and quantitative RT-PCR, we identified miR-329 as a novel regulator of NF-κB p65 mRNA that was differentially expressed in PDG -treated TLR6 [-] and TLR6 [+] trophoblast cells. [score:4]
Of these, only miR-155 and miR-329 were upregulated in PDG -treated TLR6 [-] cells and this response was reduced by the presence of TLR6 (Table 1). [score:4]
miR-329 regulates trophoblast apoptosis and NF-κB p65 and IL-6 expression. [score:4]
To date, little is known about the function of miR-329, or its targets. [score:3]
Lastly, while exposure to PDG significantly elevated caspase-3 activity in the scramble control cells, the presence of the anti-miR-329 inhibitor significantly prevented this response (Figure 5D). [score:3]
Similarly, PDG treatment significantly decreased IL-6 mRNA levels in the scramble control cells, while in the anti-miR-329 inhibitor cells, there was no effect on IL-6 mRNA (Figure 5C). [score:3]
To test this, TLR6 [-] cells were transfected with a specific anti-miR-329 inhibitor or a scramble control sequence, followed by treatment with or without PDG. [score:3]
This finding validated the microarray data by showing that the presence of TLR6 significantly reversed PDG -induced miR-329 expression in the trophoblast (Table 1 & Figure 4A). [score:3]
From these 25 miRs, trophoblast cells were found to express 8 at a detectable level: miR-7-5p; miR-186-5p; miR-155-5p; miR-22-3p; miR-185-5p; miR-138-5p; miR-329; and miR-362-3p (Table 1 and Table S1). [score:3]
For transfection studies, TLR6 [-] cells were transfected with 100nM of either an anti-miR scramble sequence control or specific inhibitors of miR-329, miR-23a or Let-7c (Mirvana, Applied Biosystems; Grand Island, NY) using siPORT [TM] NeoFX [TM] (Invitrogen). [score:3]
Thus, miR-329, miR-23a and let-7c provide a novel molecular mechanism that regulates trophoblast TLR2/TLR6 function in response to gram -positive bacterial components. [score:2]
Identification of miR-329 as a potential regulator of trophoblast NF-κB p65 mRNA. [score:2]
0077249.g004 Figure 4TLR6 [-] or TLR6 [+] trophoblast cells were treated with no treatment (NT) or PDG (80μg/ml) for 12h, after which RNA was collected and the expression of: (A) miR-329; (B) miR-23a; (C) miR-let-7c; (D) miR-149; and (E) miR-23b was measured by qRT-PCR. [score:1]
TLR6 [-] or TLR6 [+] trophoblast cells were treated with no treatment (NT) or PDG (80μg/ml) for 12h, after which RNA was collected and the expression of: (A) miR-329; (B) miR-23a; (C) miR-let-7c; (D) miR-149; and (E) miR-23b was measured by qRT-PCR. [score:1]
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3
[+] score: 13
org) was used to visualize the correlations of graphically depicting the regulation of the mRNA targets of the most interesting up-regulated mmu-miR-669c, mmu-miR-329, and down-regulated mmu-miR-688, mmu-miR-30c-1 [*], mmu-miR-201, mmu-miR-761, mmu-miR-715 microRNAs in Tff2- KO mice in a convenient way. [score:10]
Similarly, mmu-miR-329 (targeting Axin1 and Dvl2) is participating in basal cell carcinoma. [score:3]
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4
[+] score: 13
Downregulation of several miRNAs became apparent on day 7; miR-155, miR-326, miR-329 and miR-491 exhibited clearly (≤0.67-fold changes) and significantly decreased expression (P<0.05) compared with mock controls (Figure 1c and Supplementary Figures 1c and d). [score:5]
We concentrated on miR-155, miR-326, miR-329 and miR-491-5p showing stable downregulation after prolonged incubation. [score:4]
The collection included three well-known miRNAs (miR-16, miR-21 and miR-155) that have been commonly related to apoptotic signalling and cancer, [28–30] as well as three underexplored miRNAs (miR-326, miR-329 and miR-491) with accumulated targets in cancer and apoptotic pathways (Supplementary Table 3). [score:3]
[31] As shown in Figure 1e, three miR-491-5p binding sites together with two miR-329 sites and one miR-326 site were predicted (Supplementary Figure 2). [score:1]
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5
[+] score: 11
The downregulated PTTG1 -targeting miRNAs (miR-329, miR-300, miR-381, and miR-655) induced PTTG1 expression resulting in the downregulation of p53. [score:11]
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6
[+] score: 11
Other miRNAs from this paper: hsa-mir-122, hsa-mir-155, hsa-mir-362, hsa-mir-329-2, hsa-mir-603
Note that more than one miRNAs can share one target site and thus a single SNP can impact the regulation by multiple microRNAs, for example the SNP rs9893667 on gene NM_006380 (APPBP2) can influence the target site of hsa-miR-362-3p, hsa-miR-329, and hsa-miR-603 (highlighted in bold). [score:6]
This allele is the most common allele in East Asians (CHB and JPT) and CEU, but is rare in YRI, which almost exclusively possess the derived miR329 -targeted ‘G’ allele (derived allele frequency is 0.98). [score:3]
For example, the ancestral ‘A’ allele of SNP rs1050755 in SMNDC1 interfered with miR-329 regulation (Figure 1C). [score:2]
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7
[+] score: 10
Other miRNAs from this paper: hsa-mir-134, hsa-mir-206, hsa-mir-326, hsa-mir-329-2
Ectopic expression of miR-326, miR-134, miR-329, and miR-206 in NSCLC cell lines significantly suppressed cell proliferation through inhibition of cyclin D1 and up-regulation p21 [37– 40]. [score:10]
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8
[+] score: 7
By using qRT-PCR and RT-PCR, these authors predicted two miRNAs, miR329 and miR410, that could potentially target Wnt-7b, an activator of the Wnt-b-catenin pathway, thereby attenuating the Wnt-b-catenin signalling pathway in OSCC. [score:3]
Importantly, the dysregulation of the Meg-3-miR329 and -410-Wnt-7b-b-catenin signalling axis may result from exposure to betel quid chewing. [score:2]
The turquoise module contains the two miRNAs (miR-329 and miR-410) that were identified by Shiah et al. [11]. [score:1]
The information about miR-let-7c, miR-329 and miR-410 is listed in Table  1. Seventy-one of the 84 miRNAs detected by Shiah et al. are in the turquoise module and none of them are in the blue or brown modules. [score:1]
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9
[+] score: 7
stress downregulated abundance of miR-329, miR-380, miR-20a, and miR-500 (all p≤0.05; Figure 2B-C). [score:4]
C, Table of target genes for miRNAs modulated by gestational stress (miR-329, miR-380, miR-20a, and miR-500; p≤0.05), and their physiological implications. [score:3]
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[+] score: 6
OS upregulates a group of miRNAs (miR-329, miR-193b, miR-20a, miR-296, and miR-130b), which is associated with affecting 83 target genes. [score:6]
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11
[+] score: 6
In particular, hsa-mir-520e, hsa-mir-518c-5p, and all six miRNA precursors were, resultingly, downmodulated in the high risk group, while hsa-mir-329-3p, hsa-mir-302d-3p, hsa-mir-520f, hsa-mir-511-5p, hsa-mir-509-3p, hsa-mir-519a-3p, hsa-mir-521, hsa-mir-520h, and hsa-mir-499a-5p were overexpressed. [score:3]
Mir-329, by targeting oncogenic MET, reduces cell proliferation, migration, invasion, and promotes apoptosis in lung cancer cell lines [26]. [score:2]
In particular, hsa-mir-302d-3p, hsa-mir-329-3p, hsa-mir-519a-3p, and hsa-mir-520e-f were associated with multiple pathways. [score:1]
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12
[+] score: 6
The predicted MREs for the significantly -upregulated circRNAs are listed in Table 2, with hsa-miR-329-5p being the most frequently targeted miRNA by three circRNAs (i. e., hsa_circRNA_104566, hsa_circRNA_104565, and hsa_circRNA_105038) followed by hsa-miR-450b-5p, hsa-miR-205-3p, hsa-miR-95-5p, hsa-miR-339-5p, and hsa-miR-646. [score:6]
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13
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-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, mmu-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-329-2, 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
Brain stem let-7c-1, miR-17, miR-135b, miR-150, miR-199a, miR-218-1, miR-223, miR-329. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
Spinal cord miR-28, miR-217, miR-218-1, miR-329, miR-331. [score:1]
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]
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
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[+] score: 5
Haller et al. revealed the deregulation of miRNA-329, miR-370, miR-376c and miR409 expression based on the location of the tumor in gastrointestinal stromal tumors (GISTs); higher expression occurred in intestinal compared to gastric tumors [46]. [score:5]
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15
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, 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-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Among a myriad of alternative interesting expression profiles, miR-329 and miR-350 displayed a biphasic pattern of expression in the mouse epididymis (being present in the caput and cauda, but absent in the corpus), but were entirely absent in the rat epididymis and present in all regions of the human epididymis (S4 Table). [score:5]
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[+] score: 5
We did not observe any statistically significant variation in the expression levels of miR-329, miR-422a, miR-493 during development whereas these miRNAs have been described to be modulated during porcine muscle development [35]. [score:5]
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17
[+] score: 4
The only human miRNA pri-miRNA in this group was for let-7e, but the group also contained the probe for mouse miR-329. [score:1]
Our samples hybridized strongly with the probes for both mouse and rat probes for miR-290, miR-292-5p, miR-297, miR-298, and miR-329. [score:1]
Only mouse miR-329 and rat miR-329 have a known human homologue, but there were no probes for the human miR-329 on this array. [score:1]
The human miR-329 was discovered in a search for sequences homologous to the rat miR-329 [40], but in our experiments, because the sequence is not identical to the sequence for the mouse or rat homologues, the rat and mouse probes may not have hybridized to a miR-329 primary transcript. [score:1]
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[+] score: 4
Our miRNA profile (84) Chromosomal localization Fold change Reference DOWNREGULATED hsa-miR-206 6p12.2 −7.53(29) hsa-miR-219-2-3p 9q33.3 −6.64(52) hsa-miR-383 8p22 −6.56(12, 55, 56) hsa-miR-138 16q13.3/3p21.32 −5.16(12, 14) hsa-miR-323-3p 14q32.2 −4.96(12, 52) hsa-miR-122 18q21.31 −4.82 hsa-miR-105 Xq28 −4.66 hsa-miR-129-5p 11p11.2/7q32.1 −4.56(23) hsa-miR-935 19q13.43 −4.53(52) hsa-miR-329 14q32.2 −4.48 hsa-miR-129-3p 11p11.2/7q32.1 −4.43 hsa-miR-650 22q11.21 −4.19 hsa-miR-184 15q24.3 −4.14 hsa-miR-370 14q32.2 −3.99(12) hsa-miR-433 14q32.2 −3.96(29) hsa-miR-138-2* 16q13. [score:4]
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19
[+] score: 4
Kang H Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancerCell. [score:4]
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20
[+] score: 3
Target sites of two miRNA families, miR-488 and miR-329, are also very well conserved across both species. [score:3]
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[+] score: 3
MiR-329 significantly regulates cell invasion by targeting bromodomain containing 4 (BRD4) but has no effect on cell proliferation and apoptosis [51]. [score:3]
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[+] score: 3
The methylation pattern in the MEG3 DMR as well as the expression profile of miRNAs in the region can distinguish high-aggressiveness versus low-aggressiveness osteosarcoma cell lines, and the levels of miR-495, miR-329, miR-487b, miR-410, and miR-656 can predict the outcome of patients with osteosarcoma [107]. [score:3]
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[+] score: 3
Other hairpins MD5, MD17, MD157, MD244, MD366, MR175, MR201, MR268, and MR282 were aligned with hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, and hsa-miR-342-3p, respectively. [score:1]
Thus far, the 10 miRNAs, that is, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, and hsa-miR-6865-5p, do not have any known function in human and other animals. [score:1]
The utility of those 13 miRNAs, that is, hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, hsa-miR-6865-5p, and hsa-miR-342-3p, can be utilized as antiviral therapeutics against MERS-CoV infection. [score:1]
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[+] score: 3
Welten SMJ Inhibition of 14q32 MicroRNAs miR-329, miR-487b, miR-494, and miR-495 increases neovascularization and blood flow recovery after ischemiaCirc. [score:3]
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25
[+] score: 3
Other miRNAs from this paper: hsa-mir-329-2, hsa-mir-495, hsa-mir-543
An example is miR-329 family, in which any pairs of the three members (i. e. hsa-mir-543, hsa-mir-329, hsa-mir-495) share less than 20% of the targets. [score:3]
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26
[+] score: 2
For example, mir-329 appears to have diverged between human and mouse: at the syntenic location in human we find two identical copies of a miRNA distantly-related to mmu-mir-329 (HP-33 and HP-34). [score:1]
Furthermore, this cluster has a complex composition, containing other related sequences {hsa-mir-323, HP-33, HP-34, HP-35, HN-6} whereas the corresponding mouse cluster {mmu-mir-323, mmu-mir-329, MP-35, MN-7, MP-37} additionally contains a rodent-specific sequence, MN-7, which is not related to the other sequences in the cluster. [score:1]
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[+] score: 1
First, the rs2070736 creates potential binding sites for miR-362-3p and miR-329-3p in the 3′ UTR of DMWD. [score:1]
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[+] score: 1
In our research, miR-329 mimics is found to significantly decrease the phosphorylation levels of Raf-1, p38, ERK1/2, ERK5 and JNK in both U87 and U251 cells (Fig.   5a, b). [score:1]
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