&lt;p&gt;MicroRNA-188-5p Promotes Epithelial–Mesenchymal Transition by Targeting ID4 Through Wnt/β-catenin Signaling in Retinoblastoma&lt;/p&gt;

Yang, Ming; Li, Yang; Wei, Wenbin

doi:10.2147/ott.s229739

Cited by 13 publications

(14 citation statements)

References 23 publications

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“…miR-125b promoted tumor growth and suppressed apoptosis by targeting DRAM2 in RB [22]. miR-188-5p promoted epithelial-mesenchymal transition via targeting DNA binding 4 through Wnt/β-catenin signaling in RB [23]. These studies indicate that abnormal miRNA expressed may have some influence on the development of RB.…”

Section: Introductionmentioning

confidence: 79%

MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Yang

Huang

et al. 2020

Bioscience Reports

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It has been reported that miR-486-3p expression is decreased in retinoblastoma (RB) tumor tissues, however, its function in RB has been less reported. The present study aimed to explore the regulatory effects of miR-486-3p on RB cells. The expression of miR-486-3p in RB tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, proliferation, apoptosis, migration and invasion ability were determined by cell counting kit-8 (CCK-8) kit, clone formation assay, flow cytometry, scratch assay and transwell, respectively. Targetscan 7.2 and dual-luciferase reporter were used to verify target genes for miR-486-3p. The expressions of apoptosis-related proteins and ECM1 were detected by Western blot. The miR-486-3p expression was decreased in RB tissues and cells. In RB cells, overexpression of miR-486-3p inhibited cell proliferation, migration and invasion, while promoted apoptosis. Moreover, overexpression of miR-486-3p decreased Bcl-2 expression, while increased the expressions of Bax and Cleaved Caspase-3 (C caspase-3). ECM1 was the target gene of miR-486-3p, and miR-486-3p inhibited the expression of ECM1. Furthermore, ECM1 partially reversed the inhibitory effect of miR-486-3p on the proliferation, migration and invasion of RB cells. MiR-486-3p inhibited the proliferation, migration and invasion of RB by down-regulating ECM1.

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Section: Introductionmentioning

confidence: 79%

MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Yang

Huang

et al. 2020

Bioscience Reports

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“…Many miRNAs have been reported to be abnormally expressed in RB, like miR-192, miR-34a and miR-376a (34)(35)(36)(37). In RB, miR-188-5p promotes epithelialmesenchymal transition by targeting DNA binding 4 via Wnt/β-catenin signaling pathway (38). This study screened DEMs in RB samples in comparison to nontumor retina samples.…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of multiple bioinformatics studies to identify microRNA-target gene-transcription factor regulatory networks in retinoblastoma

Wang¹,

Zhu²,

Zhang³

et al. 2022

Transl Cancer Res TCR

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Background: In children, retinoblastoma (RB) is one of the most common primary malignant ocular tumors and has a poor prognosis and high mortality. To understand the molecular mechanisms of RB, we identified microRNAs (miRNAs), key genes and transcription factors (TFs) using bioinformatics analysis to build potential miRNA-gene-TF networks.Methods: We collected three gene expression profiles and one miRNA expression profile from the Gene Expression Omnibus (GEO) database. We used the limma R package to identify overlapping differentially expressed genes (DEGs) and differentially expressed miRNAs in RB tissues compared to noncancer tissues.The robust rank aggregation (RRA) method was implemented to identify key genes among the DEGs. Then, miRNA-key gene-TF networks were built using the online tools TransmiR and miRTarBase. Next, we used RT-qPCR to confirm the results. Results:We identified 180 DEGs in RB tissues compared to nontumor tissues using integrative analysis, among which 109 genes were upregulated and 71 were downregulated. Gene ontology (GO) analysis revealed that these DEGs were primarily involved with chromosome segregation, condensed chromosome and DNA replication origin binding. The most highly enriched pathways obtained in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were cell cycle, DNA replication, homologous recombination, P53 signaling pathway and pyrimidine metabolism. Furthermore, two key differentially expressed miRNAs (DEMs) were also established: let-7a and let-7b. Finally, the potential regulatory networks of miRNA-target gene-TFs were examined.Conclusions: This study identified key genes and built miRNA-target gene-TF regulatory networks in RB, which will deepen our understanding of the molecular mechanisms involved in the development of RB.These key genes and miRNAs may be potential targets and biomarkers for RB diagnosis and therapy.

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“…Yun et la found that miR-188 directly targeted PTEN to affect Wnt/β-catenin signaling in gastric cancer [38]. Yang et al demonstrated that miR-188 significantly promoted EMT by down-regulating DNA binding 4 through Wnt/β catenin signaling in retinoblastoma [39]. The difference in these studies indicated that miR-188 might regulated Wnt/β-catenin signaling through different molecules in different cancer types.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-188-5p targeting Forkhead Box L1 promotes colorectal cancer progression via activating Wnt/β-catenin signaling

Wu¹,

CHEN²,

LIU³

et al. 2021

Oncology Research

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<p>MicroRNA-188-5p Promotes Epithelial–Mesenchymal Transition by Targeting ID4 Through Wnt/β-catenin Signaling in Retinoblastoma</p>

Cited by 13 publications

References 23 publications

MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Integrated analysis of multiple bioinformatics studies to identify microRNA-target gene-transcription factor regulatory networks in retinoblastoma

MicroRNA-188-5p targeting Forkhead Box L1 promotes colorectal cancer progression via activating Wnt/β-catenin signaling

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