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miRBase |
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![]() 3 publications mentioning eca-mir-135bOpen access articles that are associated with the species Equus caballus and mention the gene name mir-135b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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Other miRNAs from this paper: eca-mir-208b, eca-mir-29a, eca-mir-29b, eca-mir-214, eca-mir-29b-2, eca-mir-29c, eca-mir-29c-2, eca-mir-26a, eca-mir-24-1, eca-mir-1-1, eca-mir-133a, eca-mir-378, eca-mir-135a, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-mir-133a-2, eca-mir-499, eca-mir-24-2, eca-mir-27b, eca-mir-155, eca-mir-486, eca-mir-135a-2, eca-mir-221
Expression profiling of miRNAs showed that miR-214 and miR-135 had significantly altered expression during myoblast differentiation with miR-214 being down-regulated and miR-135 being up-regulated more than 70-fold in differentiated cells (Fig.
[score:11]
Based on qRT-PCR results, while miR-135 was up-regulated miR-214 was down-regulated during the differentiation process.
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miR-135 may participate in the myocyte formation process through targeting unknown components (perhaps inhibitors of muscle growth) of myogenesis in addition to those targets in our prediction (activators).
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To bioinformatically predict target genes, we initially found that miR-214 and miR-135 targeted several signal molecules regulating the myogenesis process and insulin pathway such as IRS2, AKT2 and INSR (Fig.
[score:6]
Our study, for the first time, also reports that miR-135 expression was up-regulated during myogenic differentiation.
[score:6]
The aim of this study was to quantify expression changes of bioinformatically selected miR-214 and miR-135 and their targets, Insulin receptor substrates (Irs2), RAC-beta serine/threonine-protein kinase (Akt2) and insulin receptor (Insr) to better understand the role of miRNAs during the muscle differentiation process.
[score:5]
Using Target Scan 6.2 (36), miRWalk (37) and RNAhybrid (38), we generated a list of miR-214 and miR-135 candidate target genes, containing a seed site for these two miRNAs.
[score:5]
During myoblast to myocyte differentiation, miR-214 was significantly down- regulated while miRNA-135, Irs2, Akt2 and Insr were overexpressed during the process.
[score:4]
miR-214 and miR-135 are potential regulators of myogenesis and are involved in skeletal muscle development through regulating the IRS/PI3K pathway.
[score:4]
In this study, we report that miR-135 was differentially expressed and may thus be involved in skeletal muscle development.
[score:4]
We show that miR-214 and miR-135 are potential regulators of myogenesis through regulating the IRS/AKT/PI3K pathway.
[score:3]
Using a bioinformatics approach, miR-214 and miR-135 were selected according to their targets as potential factors in myoblast to myocyte differentiation induced by 3% horse serum.
[score:3]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-210, hsa-mir-181a-1, hsa-mir-224, hsa-mir-200b, hsa-mir-122, hsa-mir-142, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-200a, hsa-mir-26a-2, hsa-mir-135b, hsa-mir-18b, hsa-mir-181d, hsa-mir-92b, hsa-mir-675, eca-mir-200a, eca-mir-200b, eca-mir-34a, eca-mir-29a, eca-mir-29b, eca-mir-29b-2, eca-mir-29c, eca-mir-29c-2, eca-mir-92b, eca-mir-9a, eca-mir-200c, eca-mir-26a, eca-let-7a, eca-mir-100, eca-mir-122, eca-mir-142, eca-mir-195, eca-mir-21, eca-mir-675, eca-mir-145, eca-mir-9a-2, eca-mir-26a-2, eca-mir-17, eca-mir-18a, eca-mir-19a, eca-mir-19b, eca-mir-92a, eca-mir-126, eca-mir-181a, eca-mir-181b, eca-mir-155, eca-mir-181a-2, eca-mir-18b, eca-mir-19b-2, eca-mir-224, eca-mir-92a-2
We have revealed common small non-coding RNA molecules (miR-26a, miR-195, miR- miR-126, miR-122, miR-21, miR-155, miR-9, miR-135b, miR-29b, miR-142-3p, miR-210, miR-181, miR- 224) in HCC and CRC, which suppress the expression of multiple genes involved in tumor- stromal interactions, immune invasion and tumor angiogenesis.
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Tumorigenesis in CRC E-cadherin[41, 42] miR-135b HCC cell metastasis; CRC proliferation HSF1, MSH2[44, 45] miR-29b Apoptosis promotion Bcl-2 and Mcl-1, MMP-2[47, 48] miR-142-3p HCC and CRC proliferation RAC1, CD 133, Lgr 5, ABCG2[60, 62, 107] miR-210 HCC metastasis; overexpressed in CRC VMP1, CPEB2[51, 52] miR- 181a Oncogenic role in HCC; poor survival in patients with CRC CDX2, GATA6, NLK, EGFR[64, 65] miR- 224 Oncogenic role in HCC; prognostic marker in CRC SMAD4, API-5[49, 63]Previous studies indicated that miR-34a inhibits tumor growth, miR-21 promotes apoptosis resistance of tumor cells proliferation while the miR-200 family is strongly associated with the epithelial- mesenchymal transition (EMT) [18, 19].
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Tumorigenesis in CRC E-cadherin[41, 42] miR-135b HCC cell metastasis; CRC proliferation HSF1, MSH2[44, 45] miR-29b Apoptosis promotion Bcl-2 and Mcl-1, MMP-2[47, 48] miR-142-3p HCC and CRC proliferation RAC1, CD 133, Lgr 5, ABCG2[60, 62, 107] miR-210 HCC metastasis; overexpressed in CRC VMP1, CPEB2[51, 52] miR- 181a Oncogenic role in HCC; poor survival in patients with CRC CDX2, GATA6, NLK, EGFR[64, 65] miR- 224 Oncogenic role in HCC; prognostic marker in CRC SMAD4, API-5[49, 63] Previous studies indicated that miR-34a inhibits tumor growth, miR-21 promotes apoptosis resistance of tumor cells proliferation while the miR-200 family is strongly associated with the epithelial- mesenchymal transition (EMT) [18, 19].
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heat shock transcription factor 1 (HSF1) directly activates the miR-135b expression, consequently enhancing HCC invasiveness [44].
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Additionally, the reversion-inducing-cysteine-rich protein with kazal motifs (RECK) and ecotropic viral integration site 5 (EVI5) were identified as the functional and direct targets of miR-135b in HCC.
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Recent research identified miR-135b as a key effector of oncogenic pathways and a promising target for CRC therapy [45].
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The miR-135b blockage in CRC experimental mouse mo dels diminishes tumor evolution by suppressing the genes involved in proliferation, apoptosis and invasion.
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The development of new therapeutics against HCC could be thus facilitated by the recently identified HSF1/miR-135b/RECK&EVI5 axis in the mechanisms of HCC metastasis [17; 44].
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Other miRNAs from this paper: eca-mir-140, eca-mir-29a, eca-mir-199a, eca-mir-133a, eca-mir-193a, eca-mir-193b, eca-mir-874, eca-mir-135a, eca-mir-17, eca-mir-133b, eca-mir-133a-2, eca-mir-27b, eca-mir-135a-2, eca-mir-1249
Consistent with the known role of miRNAs in the control of bone remo deling (for review see [8]) and their involvement in key regulation pathways of bone formation and remo deling such as BMP-signaling pathway (mir-133, mir-135) [51] and Wnt-signaling pathway (mir-29a) [52], miRNA predicted targets were found to be involved in the regulation of several signaling pathways (FGF, TGFb, IGF1).
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