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• W2938993695 abstract "The aim of the present study was to characterize whether the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/miR-26a/Smad4 axis is involved in epithelial–mesenchymal transition (EMT) of lens epithelial cells (LECs). Primary human LECs were separated and cultured. Microarray analysis showed that a total of 568 lncRNAs are differentially expressed in primary HLECs in the presence of TGF- β 2 and MALAT1 is mostly significantly dysregulated lncRNAs, which is increased by nearly 17-fold. In addition, upregulation of MALAT1 and downregulation of miR-26a were detected in human posterior capsule opacification (PCO) attached LECs and the LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR (qRT-PCR). Next, our results showed that TGF- β 2 induces overexpression of EMT markers in primary HLECs via a MALAT1-dependent mechanism. The mechanism is that MALAT1 negatively regulates miR-26a and miR-26a directly targets Smad4 by luciferase reporter assays and RNA-binding protein immunoprecipitation assay. In summary, TGF- β 2 induces MALAT1 overexpression, which in turn MALAT1 acts as a ceRNA targeting Smad4 by binding miR-26a and promotes the progression of EMT of LECs." @default.
• W2938993695 created "2019-04-25" @default.
• W2938993695 creator A5051181240 @default.
• W2938993695 date "2019-04-22" @default.
• W2938993695 modified "2023-09-23" @default.
• W2938993695 title "Long Noncoding RNA MALAT1 Acts as a Competing Endogenous RNA to Regulate TGF-<i>β</i>2 Induced Epithelial-Mesenchymal Transition of Lens Epithelial Cells by a MicroRNA-26a-Dependent Mechanism" @default.
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• W2938993695 doi "https://doi.org/10.1155/2019/1569638" @default.
• W2938993695 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6501259" @default.
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