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65 publications mentioning hsa-mir-324

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-324. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 107
showed that EZH2 expression was down-regulated in glioma cells over -expressing miR-524-5p or miR-324-5p (Figure 3A). [score:8]
Furthermore, immunohistochemistry assay showed the decreased expression of EZH2 and increased expression of p21 and DKK1 after overexpression of miR-324-5p or miR-524-5p, which were consistent with the in vitro results (Supplementary Figure 1). [score:6]
We characterize two candidates, miR-524-5p and miR-324-5p, which bind to EZH2 3’UTR to down-regulate EZH2 expression, thereby suppressing glioma cell proliferation. [score:6]
MiR-524-5p and miR-324-5p exhibit a strong tumor-suppressive effect by targeting EZH2. [score:5]
Overexpression of miR-524-5p or miR-324-5p inhibits tumor growth in vitro. [score:5]
Of these miRNAs, miR-524-5p and miR-324-5p confered poor prognosis for glioma patients and inhibited glioma cell proliferation by targeting EZH2. [score:5]
EZH2 is a direct target of miR-524-5p and miR-324-5p. [score:4]
These data indicate that miR-524-5p or miR-324-5p directly modulated EZH2 expression by binding to the respective 3′UTR. [score:4]
Also MTT and colony formation assays showed that miR-324-5p overexpression suppresses cell proliferation in both U87 and U251 glioma cells (Figure 2A and 2B). [score:4]
Figure 2Overexpression of miR-524-5p or miR-324-5p inhibits tumor growth in vitro (A) Cells were treated with miR-524-5p or miR-324-5p mimics, and subjected to MTT assay. [score:4]
MiR-524-5p and miR-324-5p suppress tumor growth in an intracranial xenograft mo del. [score:3]
Taken together, these findings demonstrate that both miR-524-5p and miR-324-5p inhibited glioma malignant progression in vivo. [score:3]
Having demonstrated the profound effects of miR-524-5p and miR-324-5p on tumor suppression, we sought to examine the importance of EZH2 in miR-524-5p and miR-324-5p mediated cell proliferation. [score:3]
These suggest that EZH2 is a critical target of miR-524-5p and miR-324-5p involved in glioma cell proliferation. [score:3]
U87 cells were transfected with lentivirus overexpressing miR-524-5p or miR-324-5p and ontaining a luciferase reporter in vitro for 2 days. [score:3]
Expression of EZH2 overrides miR-524-5p and miR-324-5p function. [score:3]
Importantly, restoring EZH2 expression could override miR-524-5p and miR-324-5p function in glioma cells. [score:3]
MiR-524-5p and miR-324-5p target EZH2. [score:3]
EZH2 overexpression could eliminate miR-324-5p or miR-324-5p effects on sphere formation under TMZ treatment. [score:3]
These data indicate that miR-524-5p and miR-324-5p overexpression correlates with a significantly better survival outcome. [score:3]
Similarly, expression of EZH2 largely abrogated miR-324-5p effects on cell proliferation (Figure 4B and 4C). [score:3]
Further we check miR-524-5p and miR-324-5p expression in 158 glioma tissues. [score:3]
Over all, these findings suggest that EZH2 specific miRNAs miR-524-5p and miR-324-5p may play an important role in glioma development. [score:2]
Critical role of miR-524-5p and miR-324-5p in glioma cell proliferation. [score:1]
Thus, we explore whether miR-524-5p and miR-324-5p play key roles in TMZ resistance. [score:1]
And similar results of miR-324-5p were detected in all gliomas (P < 0.0001) and high grade glioma (P = 0.0430) (Figure 1C). [score:1]
MiR-524-5p and miR-324-5p increase TMZ chemosensitivity in glioma. [score:1]
Also, the same results of miR-324-5p in TMZ chemosensitivity were observed (Figure 5A). [score:1]
In addition, we created pGL3-WT-EZH2-3′UTR and pGL3-MUT-EZH2-3′UTR plasmids for miR-524-5p or miR-324-5p, respectively. [score:1]
Figure 3 (A) of lysates from cells transfected by miR-524-5p or miR-324-5p mimics probed with EZH2 antibody. [score:1]
MiR-524-5p and miR-324-5p were identified as key EZH2 specific miRNAs. [score:1]
Figure 4 (A) of lysates from cells transfected by miR-524-5p or miR-324-5p mimics alone, or in combination with EZH2 cDNA probed with EZH2 antibody. [score:1]
EZH2 is crucial for miR-524-5p and miR-324-5p signaling in glioma. [score:1]
Patients with low levels of miR-524-5p or miR-324-5p had a significantly worse outcome. [score:1]
We transfected miR-524-5p mimics or miR-324-5p mimics together with and without EZH2 plasmid lacking 3′UTR into glioma cells (Figure 4A). [score:1]
MiR-524-5p and miR-324-5p increases TMZ chemosensitivity in glioma. [score:1]
Among them, two miRNAs (miR-524-5p and miR-324-5p), were predicted to bind to EZH2 3’UTR. [score:1]
And miR-324-5p was also inversely associated with tumor grade (P < 0.0001). [score:1]
EZH2 reduction elevated DKK1 and p21 were elevated when cells were treated by si-EZH2, miR-524-5p and miR-324-5p mimics, as shown in Figure 5B. [score:1]
The similar results of miR-324-5p were observed (Figure 6B). [score:1]
These suggested that miR-524-5p and miR-324-5p may modulate TMZ resistance in glioma cells. [score:1]
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2
[+] score: 75
MiR-153, miR-181a and miR-324-5p were found down-regulated in brain tumor cells and proposed to function as tumor suppressors [36], [44]– [46]. [score:6]
As we identified an up-regulation of miR-153, miR-181a/a* and miR-324-5p/3p during the conversion of lt-NES cells into neurons, we became interested in whether an overexpression of these miRNAs in lt-NES cells would promote neuronal differentiation. [score:6]
In a similar analogy, miR-324-5p was found down-regulated in medulloblastoma cells and in murine self-renewing cerebellar granule cell progenitors, where it contributes to growth inhibition and differentiation by antagonizing the Hedgehog signaling [36]. [score:6]
0059011.g003 Figure 3 (A) Quantitative real-time RT-PCR analyses showing relative expression levels of mature miR-153, miR-181a, miR-181a*, miR-324-5p and miR-324-3p in lt-NES cells (I3 cell line) transduced with either LVTHM-ctr (ctr, for endogenous levels) or the respective LVTHM-miRNA overexpressing lentiviral constructs (LVTHM-miR-153, -miR-324-5p/3p, -miR-181a/a*). [score:5]
SYBR Green -based qRT-PCR analyses confirmed that expression levels of miR-153 and miR-324-5p/3p are up-regulated in neural cells compared to hES cells and further increased upon differentiation (Figure 2E, F). [score:5]
Interestingly, miR-153, miR-181a/a* and miR-324-5p/3p are all predicted to target members of the Notch pathway. [score:3]
The rate of BrdU incorporation in lt-NES cells under self-renewing culture conditions was significantly reduced by 9.41±2.53%, 22.77±6.03% and 17.73±4,76% upon overexpression of miR-153, miR-181a/a* and miR-324-5p/3p, respectively (Figure 3B and Figure S3). [score:3]
Ectopic expression of miR-153, miR-181a/a* and miR-324-5p/3p shifts lt-NES cells from self-renewal to neuronal differentiation and promotes neurite outgrowth. [score:3]
Surprisingly, overexpression of miR-324-5p/3p had no significant impact under differentiating conditions. [score:3]
Expression of miR-324-5p was shown to increase with the conversion of murine cerebellar granule cell progenitors (GCPs) into mature granule cells, where this miRNA contributes to differentiation and growth arrest by antagonizing Hedgehog signaling [36]. [score:3]
Furthermore, miR-181a as well as miR-153 and miR-324-5p were shown to act as tumor suppressors in human brain cancer cells (miR-181a, [44]; miR-324-5p, [36]; miR-153, [45], [46]). [score:3]
Overexpression of miR-153, miR-181a/a* or miR-324-5p/3p shifts lt-NES cells from self-renewal to neuronal differentiation. [score:3]
Figure S3 Overexpression of miR-153, miR-181a/a* and miR-324-5p/3p impairs the rate of BrdU incorporation in lt-NES cells. [score:3]
Overexpression of miR-153 and miR-324-5p, however, had no signifcant effect on either TH -positive or GAD -positive neurons (Figure 4C, D). [score:3]
Among the miRNAs found up-regulated in lt-NES cells and differentiating neurons compared to hES cells, we selected miR-153, miR-324-5p/3p and miR-181a/a* for further analyses. [score:3]
These data correlate with our data in lt-NES cells, where miR-324-5p/3p inhibits proliferation while promoting, to a certain degree, neuronal differentiation. [score:3]
We also observed significantly longer neurites in lt-NES-derived neurons overexpressing miR-153, miR-181a/a* or miR-324-5p/3p, compared to neurons in control cultures (Figure 3E, G). [score:2]
We validated the expression patterns of miR-181a, miR-181a*, miR-153, miR-324-5p and miR-324-3p both in I3 and in H9.2 cell lines, using Northern blotting and SYBR Green -based qRT-PCR assays (Figure 2D–F). [score:2]
We thus wondered whether the identified neural -associated miRNAs (miR-153, miR-181a/a*, miR-324-5p/3p) could also affect the development of specific neuronal subtypes with a particular focus on the dopaminergic lineage. [score:2]
Histogram showing the percentage of TH -positive neurons in untransduced lt-NES cells (I3 cell line, dashed line) and in lt-NES cells transduced with LVTHM-ctr, -miR-124, -miR-125, -miR-153, -miR-181a/a* and miR-324-5p/3p constructs, respectively, after 15 days of differentiation. [score:1]
Among these, we found miR-153, miR-324-5p/3p and the miR-181 family (Figure 1E right panel), for which evidence from other studies points to potential roles in the nervous system. [score:1]
Upon transduction of lt-NES cells with LVTHM-miR-153, LVTHM-miR-181a/a* or LVTHM-miR-324-5p/3p we observed a stable increase of the respective endogenous miRNA levels (Figure 3A). [score:1]
Taken together our data demonstrate that miR-153, miR-181a/a* and miR-324-5p/3p contribute to the transition of lt-NES cells from self-renewal to neuronal differentiation. [score:1]
Intriguingly, miR-324-5p/3p seemed to increase the number of neurons generated during propagation of lt-NES cells under self-renewing conditions (+ GF), but this effect was lost when EGF and FGF2 were withdrawn from the cultures. [score:1]
We show that miR-181a/a*, miR-153 and miR-324-5p/3p contribute to the shift from lt-NES cell self-renewal to neuronal differentiation. [score:1]
We show that miR-153, miR-324-5p/3p and miR-181a/a* contribute to shifting lt-NES cells from self-renewal to neuronal differentiation. [score:1]
Immunostainings for BrdU in lt-NES cultures (I3 cell line) transduced with LVTHM-ctr and LVTHM-miR-153, -miR-181a/a* and -miR-324-5p/3p constructs. [score:1]
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3
[+] score: 46
In particular, previous studies showed that miR-26a sensitized gastric cancer to cisplatin targeting NRAS and E [2]F [2] [22], miR-149 increased chemosensitivity of glioblastoma to Temozolomide treatment through a RAP1B -mediated remo deling of cellular cytoskeleton [23], miR-181a enhanced Adryamicin -induced apoptosis targeting Bcl-2 [24], miR-193b sensitized cancer cells to Doxorubicin targeting myeloid cell leukemia-1 (MCL-1) [25], miR-195 increased Adriamycin sensibility by downregulating RAF [26], and, finally, miR-324-3p induced drug sensitivity reducing its SMAD7 target mRNA that is associated with lung, pancreas and skin cancer [27]. [score:12]
Since miR-26a, miR-149, miR-181a, miR-193b, miR-195 and miR-324-3p are resulted to be upregulated (Figure 5) and data in literature showed their involvement in increasing drug sensitivity, we assessed also the expression levels of miR-26a and its potential target E2F2 (Hs00918090_m1) (Supplementary Figure 5). [score:8]
Conversely, miR-23a, miR-149, miR-193b, and miR-324-3p were upregulated, whereas miR-15b, miR-29a, miR-181a, miR-195, and miR-494 were downregulated (Figure 6). [score:7]
Figure 6MiRNAs deregulation was confirmed by TaqMan miRNA expression assays that specifically allowed to detect the expression levels of following miRNAs: miR-23a (Hs03659093_s1), miR-149 (Hs04231523_s1), miR-193b (Hs04231607_s1), miR-324-3p (Hs04273262_s1), miR-15b (Hs04231486_s1), miR-29a (Hs03849009_s1), miR-181a (Hs04231460_s1), and miR-195 (Hs03656088_s1) (Supplementary Figure 6). [score:5]
Figure 6 MiRNAs deregulation was confirmed by TaqMan miRNA expression assays that specifically allowed to detect the expression levels of following miRNAs: miR-23a (Hs03659093_s1), miR-149 (Hs04231523_s1), miR-193b (Hs04231607_s1), miR-324-3p (Hs04273262_s1), miR-15b (Hs04231486_s1), miR-29a (Hs03849009_s1), miR-181a (Hs04231460_s1), and miR-195 (Hs03656088_s1) (Supplementary Figure 6). [score:5]
The upregulation of other miRNAs, such as miR-149 (Hs04231523_s1), miR-181a (Hs04231460_s1), miR-193b (Hs04231607_s1), miR-195 (Hs03656088_s1) and miR-324-3p (Hs04273262_s1), was confirmed by TaqMan microRNA expression assays (Supplementary Figure 4). [score:5]
In MDA-MB-231 cells, among upregulated miRNAs there are miR-26a, miR-149, miR-181a, miR-193b, miR-195 and miR-324-3p that increase drug responsiveness. [score:4]
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4
[+] score: 38
Other miRNAs from this paper: hsa-mir-15b, hsa-mir-155, hsa-mir-338, hsa-mir-425
However, among the M. bovis BCG -downregulated miRNAs, expression of miR-324-5p and miR-338-5p was found to be SHH-regulated as the downregulation of miR-324-5p and miR-338-5p was significantly rescued in presence of a SHH inhibitor, cyclopamine (Fig. 6c). [score:12]
Among the tested miRNAs, miR-324-5p and miR-338-5p were identified as the bonafide miRNAs that target PD-L1 in a SHH -dependent manner and hence, downregulated during mycobacterial infection. [score:6]
In accordance with this observation, we found that DCs expressing miR-324-5p or miR-338-5p miRNAs displayed reduced ability to induce the surface expression as well as total protein levels of PD-L1 on M. bovis BCG infection (Fig. 6f,g). [score:5]
These results thus validate that PD-L1 is a direct target of miR-324-5p and miR-338-5p. [score:4]
The target sites located at the residues spanning from 99–106 (for miR-324-5p) and 526–533 (for miR-338-5p) of the 3′UTR of PD-L1 were identified as critical for miRNA-3′UTR interactions (Fig. 6d). [score:3]
However, the mechanism of SHH -mediated transcriptional regulation of miR-324-5p and miR-338-5p needs to be studied further. [score:2]
To establish that PD-L1 is the bonafide targets of miR-324-5p and miR-338-5p, we utilized the classical 3′UTR luciferase assays. [score:2]
The miR-324-5p and miR-338-5p binding sites were mutated in PD-L1 3′UTR by nucleotide replacements through site-directed mutagenesis using the megaprimer inverse PCR method. [score:1]
However, no significant reduction was observed when mutant construct for miR-324-5p and miR-338-5p binding on PD-L1 3′UTR was utilized (Fig. 6e). [score:1]
Transfection of a monocytic cell line THP-1 with miR-324-5p or miR-338-5p mimics markedly reduced WT PD-L1 3′UTR luciferase activity. [score:1]
MiR-324-5p, miR-338-5p mimics and negative control mimics were purchased from Ambion (Life Technologies). [score:1]
[1 to 20 of 11 sentences]
5
[+] score: 34
Interestingly, 7 of the 12 miRNAs that were up-regulated in the presence of IFN-α (miR-30b,miR-30c, miR-130a, miR-192, miR-301, miR-324-5p and miR-565) were also down-regulated in HCV -infected Huh7.5 cells. [score:7]
Seven miRNAs (miR-30b, miR-30c, miR-130a, miR-192, miR-301, miR-324-5p, and miR-565) were down-regulated in HCV-infected Huh7.5 cells (p<0.05) and subsequently up-regulated following interferon-α treatment (p<0.01). [score:7]
Of the 7 down-regulated miRNAs, miR-324-5p and miR-130a exhibited the greatest reduction in expression at a fold change (FC) of 3.50 (p = 0.0246) and 3.48 (p = 0.0110) respectively (Fig. 1C). [score:6]
MiR-324-5p (FC = 6.26, p = 0.003) and miR-489 (FC = 9.34, p = 0.006) exhibited the greatest degree of up-regulation in the presence of IFN-α while miR-30c and miR-130a demonstrated the greatest difference in expression between HCV-infected Huh7.5 cells treated with or without IFN-α (Fig. 3C). [score:6]
The GOMir tool JTarget, using five major miRNA-mRNA prediction databases, identified a list of mRNA targets for miR-30, miR-130a, miR-192, miR-301 and miR-324-5p [21]. [score:5]
Anti-miRs specific for 5 miRNAs down regulated upon HCV infection (miR-30b, miR-30c, miR-130a, miR-192, and miR-324-5p) were tested against a mock -transfected HCV [+] Huh7.5 cell control (Fig. 2). [score:2]
No effect on HCV replication was observed with miR-30b, miR-192 and miR-324-5p in vitro. [score:1]
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6
[+] score: 30
We selected, for experimental validation, targets to three of these miRNAs: hsa-miR-17-5p (one target: see below), hsa-miR-15a (two targets), and hsa-miR-324-3p (three targets). [score:9]
In some cases the true miRNA found more target sites than did, on average, the corresponding controls (miR-324-3p, Figure 1D), whereas in other cases each control, on average, found more targets than did the miRNA (miR-129, Figure 1E). [score:5]
Numbers of predicted target sites per miRNA and its control sequences for (A) miR-1 and its controls with WC nt 2–8; if miR-1 hybridized with perfect WC complementarity this would yield −30.8 kcal/mol (see Methods); (B) let-7a and imposing only the requirement of WC base pairs within nucleotide positions 2–8; let-7a perfect WC complementarity would yield −33.2 kcal/mol; (C) miR-17-5p and its controls with WC nt 2–8; perfect WC complementarity would yield −44.5 kcal/mol; (D) miR-324-3p and its controls with WC nt 2–8; perfect WC complementarity would yield −52.8 kcal/mol; and (E) miR-129 and its controls with WC nt 2–8; perfect WC complementarity would yield −41.4 kcal/mol. [score:3]
0005745.g001 Figure 1Numbers of predicted target sites per miRNA and its control sequences for (A) miR-1 and its controls with WC nt 2–8; if miR-1 hybridized with perfect WC complementarity this would yield −30.8 kcal/mol (see Methods); (B) let-7a and imposing only the requirement of WC base pairs within nucleotide positions 2–8; let-7a perfect WC complementarity would yield −33.2 kcal/mol; (C) miR-17-5p and its controls with WC nt 2–8; perfect WC complementarity would yield −44.5 kcal/mol; (D) miR-324-3p and its controls with WC nt 2–8; perfect WC complementarity would yield −52.8 kcal/mol; and (E) miR-129 and its controls with WC nt 2–8; perfect WC complementarity would yield −41.4 kcal/mol. [score:3]
Five of the target sites (hsa-miR-15a/TSPYL2, hsa-miR-15a/BCL2, hsa-miR-17-5p/TNFSF12, hsa-miR-324-3p/CREBBP and hsa-miR-324-3p/WNT9B) exhibit perfect WC complementarity in the seed regions, while has-miR-324-3p/DVL2 has one GU pair in the same region (Supplementary Figure S1). [score:3]
This selection was made on the basis of functional association with cancer (hsa-miR-17-5p, hsa-miR-15a) or predicted targets in the Wnt signalling pathway (hsa-miR-324-3p) as described in Supplementary Table S7. [score:3]
Panels B, C and D of Figure 1 show the increasingly better energy-score ranges for predicted targets of let-7a, miR-17-5p and miR-324-3p. [score:3]
Although the binding site of hsa-miR-324-3p/DVL2 has very low (stable) free energy, the presence of a GU pair in the seed region means that binding at the 3′ end of the miRNA would have to be optimal to compensate (if indeed 3′-end hybridization can compensate at all); in this case, however, two unpaired bases and two GU pairs are predicted in the 3′ end, blocking even the possibility of adequate compensation. [score:1]
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7
[+] score: 21
Other miRNAs from this paper: hsa-mir-218-1, hsa-mir-218-2
We further observed downregulation of cellular miR-324-5p, which we showed to putatively target both E-cadherin and beta-catenin, and thus its downregulation would lead to increased expression of the target proteins [11]. [score:13]
In agreement with these findings, we also observed downregulation of miR-324-5p, a cellular microRNA predicted to target both E-cadherin and N-cadherin expression [11]. [score:8]
[1 to 20 of 2 sentences]
8
[+] score: 19
The expression of serum miRNA-4522, miRNA-324-3p, and miRNA-6767-5p was down-regulated in the women with PCOS compared with the control subjects (fold changes in the ratio of the expression in women with PCOS/the expression in control subjects = 0.63, 0.65, and 0.66, respectively). [score:9]
The expression of miRNA-324-3p was down-regulated in patients with KRAS-variant endometrial tumors [33], and miRNA-324-3p was suggested as a prognostic biomarker of endometrial cancer [34]. [score:6]
Serum miRNA-4522, miRNA-324-3p, and miRNA-6767-5p were down-regulated in women with PCOS compared with controls in the microarray analysis. [score:3]
Except for miRNA-324-3p, the miRNAs identified in our study had not been previously detected. [score:1]
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9
[+] score: 18
In addition, both miRNA-324-5p targeting gli1 and miRNA-326 regulating the expression of Smo and Gli1 by cooperating with miRNA-324-5p 33 were highly expressed in LX2, but not in CP-MSC (Fig. 5A). [score:8]
The expression of both miRNA-324-5p and miRNA-326 inhibiting gli1 was lower in CP-MSCs than in healthy human liver or LX2 (Fig. 5A). [score:5]
It was previously reported that miRNA-125b, miRNA-324-5p and miRNA-326 targeted Hh target genes in human medulloblastoma cell lines 33. [score:5]
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10
[+] score: 18
Interestingly, a strong upregulation of N-cadherin, which is a predicted target of miR-324-5p, and downregulation of PDZD2, which is target of miR-146a, have been shown [127]. [score:11]
miRNAs microarray analysis showed that, in the presence of E5, miR-324-5p was constantly downregulated and miR-146a was constantly found upregulated in HaCaT-E5 cells at all time points examined [127]. [score:7]
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11
[+] score: 16
Comparing among the group between non-responder and responder, miR-4299 and -939 were the most up-regulated and miR-196b, miR-324-5p and 455-3p were the most down-regulated miRNAs. [score:7]
Secondly, in most of miRNAs we identified (miR-196b, miR-4299, miR-324-5p, miR-455-3p and miR-939), the potential linkage between their expression and chemoresistance was already established; then some of them were identified for the first time. [score:3]
A validation study was done to corroborate a subset of the results, including expression levels of miR-4299, miR-196b, miR-324-5p, miR-455-3p and miR-939, through analyzing stage IV colon adenocarcinoma tissues (not responding and responding to the chemotherapy) with laser capture microdissection and quantitative real-time PCR. [score:3]
Fig.  2 Dots indicate of the relative quantification (RQ) values of miRNA expression levels (a miR-4299, b miR-196b, c miR-324-5p, d miR-455-3p, e miR-939), normalized by U6. [score:3]
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12
[+] score: 16
The top 20 miRNAs significantly up- or down-regulated in Exo [Hypoxic] compared to Exo [Normoxic] are listed in Table 1. Nine miRNAs were expressed at a significantly lower level in Exo [Hypoxic] compared to Exo [Normoxic]: miR-521 (Fold change = 0.0005), miR-27a (Fold change = 0.24), miR-324 (Fold change = 0.446), miR-579 (Fold change = 0.448), miR-502 (Fold change = 0.396), miR-222 (Fold change = 0.232), miR-135b (Fold change = 0.325), miR-146a (Fold change = 0.456) and miR-491(Fold change = 0.482). [score:4]
A later study highlighted the role of miR-324-5p in suppression of hepatocellular carcinoma by counteracting extracellular matrix degradation [31]. [score:3]
Expression of miR-521, miR-885, and miR-324 in non-neoplastic and neoplastic prostate cells and their exosomes. [score:3]
In colon cancer, dysregulation of miR-324-5p resulted in macrophage dysfunction [30]. [score:2]
RNU6-2 (U6) was used as an internal control and q-PCR results were represented as a fold change relative to normoxic or healthy subjects for miR-521 (A), miR-885 (B) and miR-324 (C). [score:1]
Levels of miR-521, miR-885, and miR-324 in LNCaP cells, Exo [Hypoxic] and exosomes derived from the serum of PCa patients. [score:1]
Furthermore, arrays showed that miR-324 levels are decreased in Exo [Hypoxic]; however, q-PCR results showed an increase in miR-324 in Exo [Hypoxic]. [score:1]
Similar to Exo [Hypoxic], we observed higher miR-324 levels in exosomes in serum of PCa patients versus healthy individuals (Figure 6C). [score:1]
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13
[+] score: 15
mRNA, messenger RNA Table 1circRNA-miRNA-mRNA network elements for those circRNA-miRNA interactions predicted by both miRanda and RNAHybrid, with a miRanda match score > = 180 and mRNA targets that are differentially expressed (uncorrected P < 0.05) with log2(fold change) >= 2 or =< − 2 (high stringency network) Circular RNA microRNA target Number of binding sites predicted Target genes (differentially expressed) X:47,431,299–48,327,824 hsa-miR-139-5p 6 NOTCH1, STAMBP, TPD52 8:144,989,320–145,838,888 hsa-miR-320a 2 METTL7A, PBX3, PLS1, SEC14L1, VCL, VIM, VOPP1, YPEL2 8:144,989,320–145,838,888 hsa-miR-320b 2 RTKN, VCL, VOPP1 X:47,431,299–48,327,824 hsa-miR-449a 1 BAZ2A, MFSD8, NOTCH1, TSN, ZNF551 8:144,989,320–145,838,888 hsa-miR-125a-3p 1 ANKRD62, C15orf40, COL18A1, MFSD11, MPEG1, MUL1, TTC31, WDR12, ZNF641 X:47,431,299–48,327,824 hsa-miR-125a-5p 1 CD34, MEGF9, PANX1, RIT1, TP53INP1 8:144,989,320–145,838,888 hsa-miR-125a-5p 1 CD34, MEGF9, PANX1, RIT1, TP53INP1 X:47,431,299–48,327,824 hsa-miR-324-5p 1 FOXO1, MEMO1, PSMD4, SMARCD2 14:23,815,526–24,037,279 hsa-miR-142-3p 1 BTBD7, CLDN12, CPEB2, CSRP2, DAG1, KIF5B, PTPN23, WHAMM 4:88,394,487–89,061,166 hsa-miR-133b 1 FAM160B1 4:88,394,487–89,061,166 hsa-miR-448 1 DDIT4, PURG 4:88,394,487–89,061,166 hsa-miR-339-5p 1 AXL, HLA-E, METTL7A, ZNF285, ZNRF3 MetaCore pathway analysis on the 255 filtered differentially expressed target genes from the previous analysis revealed 112 perturbed pathways (corrected P < 0.01; Table  2, Additional file  8: Table S5). [score:15]
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14
[+] score: 14
Among the differentially expressed miRNAs, up-regulated miRNAs including miR-34b-5p, miR-578, miR-1304, and miR-324-5p and down-regulated miRNAs including miR-7-5p, and miR-34b-3p were analyzed using primers for mature mRNAs (B). [score:8]
Expression of miR-578, miR-1304, and miR-324-5p showed 1.5, 2.4, and 3.7 fold increase, respectively, but did not reach statistical significance. [score:3]
The differential expression of miRNAs from array experiments was confirmed by further analysis of selected miRNAs, including miR-7-5p, miR-34b-3p, miR-34b-5p, miR-578, miR-1304, and miR-324-5p, using qRT-PCR. [score:3]
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15
[+] score: 12
Downregulation of, miR-193b, miR-324-5p, miR-326, and miR-338-3p in human cancers de-repress Smoothened and promotes tumor proliferation and invasion through aberrant Hedgehog signaling activation. [score:4]
Smoothened is a direct target of, miR-193b, miR-324-5p, miR-326, and miR-338-3p. [score:4]
Smoothened is a direct target of (Ferretti et al., 2008), miR-193b (González-Gugel et al., 2013), miR-324-5p (Ferretti et al., 2008), miR-326 (Ferretti et al., 2008), and miR-338-3p (Huang et al., 2011b). [score:4]
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[+] score: 12
As well, several of the down-regulated miRNAs may also interact with targets in a variety of unconventional ways [55], [56]: for example, mir-10a can enhance translation of 5′-TOP proteins responsible for regulating global translation of transcripts [57] and mir-324-5p lies upstream of the nearby PSD95 gene and may affect its transcription [58]. [score:11]
In addition, three pairs of miRNAs are encoded at distances greater than 100 kb but still lie within the same chromosomal region: a) mir-424 and 20b at Xq26.2-3, 377 kb apart; b) mir-142 and 301a at 17q22, 820 kb apart; and c) mir-324-5p and 497 at 17p13.1, 205 kb apart. [score:1]
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[+] score: 11
Upregulation of miRNAs from the miR-17 ∼ 92 cluster (in this work miR-18a, 19a, and 92a-1) and downregulation of miR-324-5p were previously described in human MB of the SHH subgroup (12, 13). [score:7]
2 −2.03(52) hsa-miR-134 14q32.2 −2.03(12, 29) hsa-miR-346 10q23.2 −2.01(12, 13) hsa-miR-324-5p 17p13.1 −2.00(12, 50) UPREGULATED hsa-miR-199b-3p 9q33.3 4.56(12) hsa-miR-199a-3p 19p13.2/1q24.1 4.49 hsa-miR-199a-5p 19p13.2/1q24.1 4.14(28) hsa-miR-21 17q22 3.70(12– 14, 29, 31) hsa-miR-214 1q24.2 3.59 hsa-miR-19a 13q31.3 3.11(12– 14) hsa-miR-92a-1* 13q31.3/Xq26.2 3.06 hsa-miR-214* 1q24.2 2.93 hsa-miR-34a 1p36.23 2.78(13, 30, 53) hsa-miR-18b Xq26.2 2.74 hsa-miR-422a 15q22.2 2.72(14) hsa-miR-34a* 1p36. [score:4]
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[+] score: 10
The relative expression level of each miRNA was calculated using the 2 [−ΔΔCt] method, in which each miRNA is quantified relative to the expression of one reference miRNA, chosen among hsa-miR-324-5p (ID 000539), hsa-miR-320a (ID 002277) and hsa-miR-330-3p (ID 000544) according to the target miRNA level of expression, and a calibrator sample. [score:7]
e. m. value of hsa-miR-137, hsa-miR-376c-3p, hsa-miR-203a-3p and hsa-miR-146a-5p relative expression level in two series of biological replicates from the first microfluidics arrays (five control and five FD hOE-MSCs) and the second arrays (four healthy control and four FD hOE-MSCs), respectively normalized by hsa-miR-320a (for both hsa-miR-137 and hsa-miR-376c-3p), hsa-miR-330-3p and hsa-miR-324-5p. [score:3]
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[+] score: 10
For the first set of MSCs only 3 miRNAs (miR-324-3p, miR-494-3p, and miR-1260a) were observed to be statistically significant (p < 0.05) between passages 3 and 7. For the second set of MSCs, 7 miRNAs (let-7i, miR-25-3p, miR-106b-5p, miR-130b-3p, miR-199a-5p, miR-365a-5p, and miR-1260a) were statistically significant between passages 4 and 8. MiR-1260a was found to be significantly different between early and late passages for both MSC sets; however, it was upregulated at passage 7 for the first MSC set and downregulated at passage 8 for the second MSC set. [score:7]
In evaluating early passage MSCs (13 cell lines) against the 4 cell lines of the mesoderm lineage, 5 miRNAs (miR-15b-5p, miR-25-3p, miR-320d, miR-324-3p, and miR-494-3p) were observed to be significantly upregulated (p < 0.05) in the non-MSC lines. [score:2]
Out of the 13 miRNAs being evaluated for new consensus miRNAs in MSCs, 8 miRNAs had detectable expression in both the microarray and experiments (miR-22-3p, miR-27a-3p, miR-34a-5p, miR-193b-3p, miR-320b, miR-324-3p, miR-494, and miR-1260a). [score:1]
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[+] score: 10
Other miRNAs from this paper: hsa-mir-203a, hsa-mir-205, hsa-mir-146a, hsa-mir-203b
Importantly, up-regulation of human miR-146a and down-regulation of human miR-203 and miR-324-5p, with subsequent regulation of their known and predicted target genes, was shown. [score:10]
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[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
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[+] score: 9
Of these, 14 (miR-23b, miR-28, miR-98, miR-103, miR-107, miR-193a,0, miR-324-5p, miR-324-3p, miR-331, miR-374, miR-432, miR-502, and miR-660) were upregulated and 6 (miR-31, miR-451, miR-452, miR-565, miR-594 and miR-659) were downregulated. [score:7]
[27]↓quail myoblasts diff, ↓ C2C12 diff [29] ↓ C2C12 diff [28] ↓ muscle development [32]40miR-320↓(this study)↑ pMyo diff [33]  41 miR-324-3p (n)↑↑(this study)   42 miR-324-5p (n)↑(this study)   43 miR-331 (n)↑(this study)-  44miR-339↓(this study)↑ C2C12 diff [33] ↑ pMyo diff [33]  45miR-361↑(this study)↑ pMyo diff [33]  46 miR-362↑↑(this study)↑ C2C12 diff [28]  47 miR-374 (n)↑(this study)   48 miR-432 (n)↑(this study)   49 miR-451 (n)↓↓↓(this study)   50 miR-452 (n)↓↓(this study)   51 miR-500↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  52 miR-501↑↑↑(this study)↑ C2C12 diff [28, 33]  53 miR-502 (n)↑↑(this study)-  54 miR-503↑(this study)↑ C2C12 diff [19, 28, 33] ↑ pMyo diff [33]  55 miR-532↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  56↓↓ pMyo diff. [score:2]
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[+] score: 9
Six miRNAs, 3 less expressed (miR-324-3p, miR-516a-3p, miR-659-3p) and 3 more expressed (miR-137, miR-301a-3p, miR-873-5p) in BM-infiltrating cells than in primary tumors, were significantly differentially expressed also in this new set of samples (Table 2). [score:7]
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
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24
[+] score: 8
In this study we also observed that decreased miR-324-5p expression levels correlated with increased left and right hippocampal volume; interestingly miR-324-5p promotes neuronal differentiation and it may contributes to the development of defined neuronal subtypes [63], [64]. [score:4]
Specifically, six miRNAs (miR-185, miR-15b-3p, miR-363, miR-324-5p, miR-361-5p, and miR-194) were dysregulated in individuals with 22q11DS when examining left hippocampal volume (Figure 5 ), and also with right hippocampal volume (Figure 6 ), while the expression level of two miRNAs (miR-361-5p, and miR-194) significantly decreased with increased whole brain volume (Figure 7 ). [score:4]
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25
[+] score: 8
Stem-loop real-time PCR was used to further examine the expression of the 5p arm and 3p arm miRNAs of miR-324 and miR-455 in 10 paired (tumor and adjacent normal) breast cancer tissue samples. [score:3]
The ratio of 5p to 3p expression in miR-324 was increased significantly in breast cancer cells. [score:3]
In Figure 4, the NGS data showed that the expression ratios of the 5p arm to 3p arm miRNAs of miR-324 and miR-455 were individually increased and decreased in the tumor, respectively, compared with in normal tissue. [score:2]
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[+] score: 8
In contrast, miR-196a/b/c, miR-224 and miR-324-3p were found to be downregulated, hence their low expression may also be indicative of recovery. [score:6]
Except for miR-324-3p [62], all of them have been found to be involved in TGF-β signaling pathway regulation. [score:2]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-221, hsa-mir-940
Subsequently, using BLAST and in silico algorithm -based predictions, we identified three microRNAs, hsa-miR-324-3p, hsa-miR-221, and hsa-miR-940, that were differentially expressed between DU-145 and PWR-1E cells and could potentially target MIEN1 3′UTR (Additional file 2: Figure S2A and S2B) [20, 21]. [score:5]
The expression of miR-221 and miR-324-3p were neither consistently higher in the immortalized cells compared to the cancer cells, nor were they significantly different, together indicating that miR-940 may be the most relevant regulator of MIEN1 among the three miRNAs. [score:3]
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[+] score: 7
miR-324, together with four other miRNAs that show isoform differences in tumor versus non-tumor samples (miR-106b, miR-335, and miR-411), also exhibited variations in the major arm of the pre-miRNA expressed as a miRNA (Table S2, S3, S4, S6). [score:3]
In particular, 5′ end sequence heterogeneity may have functional implications as there are observable differences in the dominant isoforms for a few miRNAs (miR-335, miR-106b, miR-324) expressed in glioblastomas. [score:3]
Interestingly, the dominant form of miR-324-3p was consistent with the miRNA sequence reported in miRBase; however, in non-tumor brain, we observed a significant number of reads mapping to a miR-324-3p isoform that was two nucleotides longer at the 5′ end (Table S7). [score:1]
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[+] score: 7
To verify the accuracy of microarray results we chose a selection of miRNAs from up-regulated (miR-10a-5p, miR-196b-5p, miR-352 and miR-324-3p) and down-regulated (miR-128a-3p) categories for confirmation using the method. [score:7]
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[+] score: 7
Furthermore, mirPRo reported that hsa-miR-324-5p is up-regulated significantly (see human data alignments in) whereas miRDeep2 determined that it does not have a significant differential expression. [score:6]
mmu-miR-152-3p exemplifies the case (Δ/−) while has-miR-324-5p exemplifies the case (Δ/+) shown in Fig. 2. The alignment results from miRDeep2 are presented in Supplementary Data 12– 21. [score:1]
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[+] score: 6
not significant Many Th1- and Th2-type inflammation-linked miRNAs, including miR-155, miR-146, and miR-324-5p, appear to be conserved in both mouse and human macrophages and are induced by LPS or IL-4, suggesting that the regulation of miRNA expression and function during classic or alternative macrophage activation is conserved [15, 18, 20, 24, 75]. [score:4]
We observed that the majority of IL-4-regulated miRNAs were strictly STAT6 -dependent in mouse macrophages, including miR-342-3p, miR-125a-5p, and miR-99b-5p, as well as the previously studied miR-511-5p and miR-324-5p. [score:2]
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[+] score: 6
Among the listed profiles of differentially up-regulated miRNA, it was found that miR-141, miR-181c*, miR-210, miR29b, miR-324-5p, and miR-663 were up-regulated (>1.5-fold, p<0.05) at 3-hour post-infection with subtype H5 as compared with non-infected control cells. [score:6]
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33
[+] score: 6
Xu J Ai Q Cao H Liu Q MiR-185-3p and miR-324-3p predict radiosensitivity of nasopharyngeal carcinoma and modulate cancer cell growth and apoptosis by targeting SMAD7Med Sci Monit. [score:3]
Twelve miRNAs in group 5 (miR-196b, miR-485-3p, miR-589, miR-324-3p, miR-342-3p, miR-92a1#, miR-155, miR-146b, miR-142-3p, miR-1260, miR-143, and miR-142-5p) have strong loading (absolute value ≥ 0.8). [score:1]
The majority of these miRNAs have been reported as prognostic markers in different types of cancers, while miR-324-3p, miR-155, miR-142-3p, and miR-143 have been identified as prognostic indicators in head and neck tumors of different locations [69– 73]. [score:1]
Twelve miRNAs in this group (miR-196b, miR-485-3p, miR-589, miR-324-3p, miR-342-3p, miR-92a-1#, miR-155, miR-146b, miR-142-3p, miR-1260, miR-143, and miR-142-5p) seem to be influential on patient prognosis. [score:1]
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34
[+] score: 6
Other miRNAs from this paper: hsa-let-7d, hsa-mir-107, hsa-mir-215, hsa-mir-224, hsa-mir-15b
Fish-oil exposure also prevented downregulation of five miRNAs (let-7d, mir-15b, miR-107, miR-109 and miR-324–5p) by AOM treatment, and had the overall strongest reducing effect on the numbers of differentially expressed miRNAs. [score:6]
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35
[+] score: 6
Other miRNAs from this paper: hsa-mir-31, hsa-mir-183, hsa-mir-143, hsa-mir-155
Amongst miRs identified to potentially target IL13RA1, we selected a subset previously reported to be dysregulated in inflammatory bowel disease (Figure 2a and Table S1): miR-155-5p [28, 29], miR-31-5p [28, 30], miR-183-5p [28] and miR-324-3p [30]. [score:6]
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[+] score: 6
In this study, five miRNAs (miR-29a, miR-29b, miR-126*, miR-127-3p, miR324-3p) were found upregulated and four (miR-188-5p, miR-25, miR-320a, miR-346) downregulated in both quiescent and active UC compared to healthy controls (Fasseu et al., 2010). [score:6]
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37
[+] score: 5
Evaluating the miRNA profile in a human vascular endothelial cell line (EAhy926) infected with DENV-2 (TR1751 strain) by microarray and qRT-PCR, 12 miRNA candidates were found to be up-regulated (miR-3178, miR-324-3p, miR-937, miR-3195, hsv1-miR-H6-3p, kshv-miR-K12-12*, let-7a-2*, miR-20b*) and down-regulated (miR-21*, miR-2116, miR-142-3p, miR-223). [score:5]
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38
[+] score: 5
Interestingly, all these miRNA target sites mapped to the viral RNA regions encoding viral accessory proteins: the nef gene harbored target sites for miRNAs miR-29a and miR-29b, the vpr for miR-149, the vif for miR-324-5p, and vpu for miR-378 (Figure 2 and Table 1). [score:5]
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39
[+] score: 5
Other miRNAs from this paper: mmu-mir-324
2004.09.003 15380510 9. Song L. Liu D. Zhao Y. He J. Kang H. Dai Z. Wang X. Zhang S. Zan Y. Sinomenine inhibits breast cancer cell invasion and migration by suppressing NF-kappa B activation mediated by IL-4/miR-324-5p/CUEDC2 axisBiochem. [score:5]
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40
[+] score: 5
In this previous research, we showed that miR-324-5p and miR-326 targeting gli1 mRNA were highly expressed in activated LX2 cells. [score:5]
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41
[+] score: 5
The remaining four miRNAs (miR-324-5p, miR-330-3p, miR-509 and miR-625) caused a slight reduction in the expression levels of the truncated isoform of NTRK3 (maximum 15%), but none of them reached statistical significance. [score:3]
In the case of pGL4.13-TR, the luciferase activity was significantly reduced by 8 miRNAs (Figure 1A), all of which were predicted by at least one program: miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p. [score:1]
Luciferase-validated miRNAs were therefore transfected into either undifferentiated (miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p) or differentiated SH-SY5Y cells (miR-151-3p and miR-185), and protein levels were assessed by western blotting 72 h after transfection. [score:1]
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42
[+] score: 5
Several miRNAs (miR-29a, miR-29b, miR-149, miR-378, miR-324-5p) targeted to the human immunodeficiency virus (HIV) genome and inhibited viral infection in T cells [14]. [score:5]
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43
[+] score: 5
Other miRNAs from this paper: hsa-mir-198, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3
miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma. [score:5]
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44
[+] score: 4
The most common down-regulated miRNAs were miR-30a-5p (6 profiles), followed by miR-139-5p, miR-187-3p, miR-551b-3p, miR-140-3p, miR-324-5p, miR-33-5p, miR-218-5p, miR-378a-3p and miR-29c-5p (Supplementary Table  S4). [score:4]
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45
[+] score: 4
044hsa-miR-18b2.20.014hsa-miR-423-5p1.70.048hsa-miR-932.10.014hsa-miR-1911.50.049hsa-miR-548b-5p2.30.015Downregulated miRNAs  hsa-miR-252.10.015hsa-miR-885-5p-4.20.00011hsa-miR-324-3p2.30.017hsa-miR-874-5.80.00018hsa-miR-3262.60.017hsa-miR-486-3p-4.60.00040hsa-miR-18a3.10.017hsa-miR-299-5p-4.20.0020hsa-miR-20b2.00.017hsa-miR-488-3.90.0063hsa-miR-1942.80. [score:4]
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46
[+] score: 4
Another critical cancer suppressor gene TP53 was regulated by miR-454-3p in KIRC, and by miR-324-5p and -222-3p in KIRP. [score:4]
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47
[+] score: 4
MiRNAs miR-324-3p (1.73x), miR-1227 (1.95x), miR-362-3p (1.85x), miR-99b-3p (2.21x), miR-19b-1-5p (4.11x), miR-628-3p (2.77x), miR-26a-1-3p (42.47x), miR-576-3p (2.49x) and miR-27a-5p (108x) were up-regulated, in OROV-infected cells relative to uninfected cells. [score:4]
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48
[+] score: 4
Ectopic expression of miR-153, miR-181a/181a*, and miR-324-5p/3p shifted lt-NES cells from self-renewal to neuronal differentiation. [score:3]
This extensive profiling pointed to additional miRNAs enriched in differentiated neurons, miR-125b, miR-153, miR-181a/181a*, and the cluster miR-324-5p/3p. [score:1]
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49
[+] score: 4
Down-regulation of Dicer was followed by decreased production of several miRNAs (miR1301, miR1249, miR1227, miR532-3p, miR625, miR1827, miR324-5p) as assessed by real-time PCR (data not shown). [score:4]
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50
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
Levels of eight circulating serum miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-206, miR-140-5p, miR-455-5p, and miR-362-3p) were significantly higher in sera of patients with enteroviral infections (215). [score:1]
The combination of six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p, and miR-362-3p) generated a biosignature that could distinguish enteroviral patients and HC. [score:1]
In addition, a panel comprising miR-143, miR-324-3p, and miR-545 had moderate ability in discriminating patients infected with CVA16 from those with EV71 (215). [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-21, hsa-mir-34a, hsa-mir-193b, hsa-mir-615
We found a possible binding-site to the hsa-mir-324-3p, a cellular miRNA targeting Cdk5rap2 gene, in the ZIKV genomes. [score:3]
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[+] score: 3
Only five miRNAs were intronic in genes that play a role in the mRNA subtype classification (hsa-mir-324 in ACADVL, hsa-mir-153 in PTPRN2, hsa-mir-934 in VGLL1, hsa-mir-595 in PTPRN2, hsa-mir-744 in MAP2K4), demonstrating that the miRNA differential expression is not merely a recapitulation of the mRNA classification. [score:3]
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[+] score: 3
miR-let-7d, miR-324, miR-16-2-3p and miR-126 were used as normalizers based upon their universal expression in all samples and high stability in the profiling dataset, as assessed by Normfinder [31]. [score:3]
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54
[+] score: 3
Lerman et al. observed the expression of the following miRNAs in psoriatic lesion skin: hsa-miR-149, hsa-miR-150, hsa-miR-210, hsa-miR-220, hsa-miR-326, has-miR-324-5p, hsa-miR-342, hsa-miR-326, hsa-miR-328, hsa-miR-345, hsa-miR-346, and hsamiR-197 [20]. [score:3]
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[+] score: 3
Of the 22 non-coding transcripts, we identified 2 differentially expressed genes in the proximal tail categorized within the miRNA precursor families miR-133 and miR-324. [score:3]
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56
[+] score: 3
The miRNAs miR-324-3p, miR-17-5p, miR-30a-5p, miR-93-3p and miR-196a-5p were densely connected, each having more than 17 synergistic interactions with other miRNAs in the network. [score:1]
Our further analysis detected substantial involvement of the miRNAs miR-324, miR-93, miR-615 and miR-1 in breast cancer, which was not known previously. [score:1]
In addition to those hub miRNAs, we found hub miRNAs with no previous association in breast cancer, including miR-615-3p, miR-1, miR-484, miR-192-5p and miR-324-5p. [score:1]
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[+] score: 3
In their study, miR-125b, miR-324-5p, and miR-326 were demonstrated as the suppressors of sonic hedgehog signaling (Shh) pathway and MB cells showed increased proliferation when these microRNAs were diminished. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Another subgroup of miRNAs displayed an opposite pattern, i. e. decreased expression during latency: miR-7a-1-3p, miR-107-3p, miR-138-5p, miR-139-3p, miR-186-5p, miR-204-5p, miR-222-3p, miR-324-3p and miR-505-3p were significantly decreased during latency (peak at 4 days after SE), then gradually returned to control levels (Fig. 2, Supplementary Fig. S2). [score:3]
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[+] score: 2
Further analysis revealed that combined six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p and miR-362-3p) could discriminate patients with enterovirus infections from healthy controls. [score:1]
In addition, six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p and miR-362-3p) possessed the ability to discriminate patients with enterovirus infections from healthy controls [22]. [score:1]
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[+] score: 2
We and others have described several miRNAs that are involved in MB development, including miR-125b, miR-324-5p, miR-326 and miR-199b-5p [6], [7], [8]. [score:2]
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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-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-100, hsa-mir-101-1, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-215, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-194-1, hsa-mir-195, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-130b, hsa-mir-302c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-451a, hsa-mir-483, hsa-mir-484, hsa-mir-486-1, hsa-mir-500a, hsa-mir-92b, hsa-mir-595, hsa-mir-596, hsa-mir-421, hsa-mir-378d-2, hsa-mir-744, hsa-mir-885, hsa-mir-939, hsa-mir-940, hsa-mir-1229, hsa-mir-1233-1, hsa-mir-1290, hsa-mir-1246, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-4286, hsa-mir-500b, hsa-mir-1233-2, hsa-mir-3935, hsa-mir-642b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j, hsa-mir-486-2
Another study on exosomal miRNAs in esophageal adenocarcinoma confirmed that a multi-biomarker panel of small noncoding RNAs (RNU6-1/miR-16-5p, miR-25-3p/miR-320a, let-7e-5p/miR-15b-5p, miR-30a-5p/miR-324-5p, and miR-17-5p/miR-194-5p) demonstrated enhanced specificity and sensitivity over single miRNA ratios to distinguish esophageal adenocarcinoma from controls and Barrett’s esophagus. [score:1]
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[+] score: 1
As in rodents, this analysis identified the presence of an IGF/Insulin-activated microRNA node comprised of miR-1913, 423, 155, 130a, and 10 (red on diagram) as well as miR-324 (pink), which was shared with the rat IGF/Insulin node (Figure 3E ). [score:1]
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[+] score: 1
The nine stress-responsive miRs, miR-142-5p, miR-19b, miR-1928, miR-223-3p, miR-322 [∗], miR-324, miR-421-3p and miR-463 [∗] identified may have potential as biomarkers for PTSD. [score:1]
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However, In addition to the repressive effect of miR-21-5p on MYC, we observed five decreased miRNAs (let-7b-5p, miR-92a, miR-320b, miR-324-3p and miR-423-5p) to exhibit significant positive correlations with MYC. [score:1]
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In the 67 APAP-early patients, miR-122-5p identified subsequent liver injury when normalized by any of the 6 endogenous miRNA normalizers described above (miR-122-5p area under ROC curve normalized by miR-1913, 0.97 (95% CI 0.92–1.01); miR-671, 0.96 (0.92–1.01); miR-1287, 0.95 (0.90–1.00); let7-d, 0.94 (0.89–1.00); miR-1260, 0.93 (0.88–1.00); miR-324, 0.93 (0.87–1.00) miR-122-5p ROC-AUC significantly larger than all other miRNAs – P < 0.05). [score:1]
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