MicroRNA miR-29c-3p modulates FOS expression to repress EMT and cell proliferation while induces apoptosis in TGF-?2-treated lens epithelial cells regulated by lncRNA KCNQ1OT1 - 28/08/20
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Highlights |
• | MiR-29c-3p was decreased in ARC tissues and cells. |
• | MiR-29c-3p suppressed the progression of ARC. |
• | KCNQ1OT1 sponged miR-29c-3p to regulate FOS expression. |
• | KCNQ1OT1 regulated the progression of ARC through miR-29c-3p/FOS axix. |
Abstract |
Age-related cataract (ARC) is a main cause of blindness for elderly people. MicroRNA hsa_miR-29c-3p (miR-29c-3p) was implicated in many biological processes in complicated diseases. However, the biological mechanism of miR-29c-3p in ARC is still undefined. Quantitative real-time polymerase chain reaction (qRT-PCR) showed that miR-29c-3p was lowly expressed, while FBJ murine osteosarcoma viral oncogene homolog (FOS) and KCNQ1 overlapping transcript 1 (KCNQ1OT1) were highly expressed in cataract tissues and in TGF-β2-treated SRA01/04 cells. Western blot assay indicated that TGF-β2 could promote epithelial-mesenchymal transition (EMT). Moreover, our data suggested that miR-29c-3p overexpression suppressed EMT, cell proliferation and promoted apoptosis in TGF-β2-treated SRA01/04 cells. The dual-luciferase reporter assay verified that FOS was a target of miR-29c-3p and miR-29c-3p was directly targeted by KCNQ1OT1. Furthermore, KCNQ1OT1 could regulate FOS expression by sponging miR-29c-3p. Functional assays revealed that miR-29c-3p regulated FOS to repress EMT, cell proliferation and facilitate apoptosis in TGF-β2-treated SRA01/04 cells mediated by KCNQ1OT1. In conclusion, KCNQ1OT1/miR-29c-3p/FOS axis played a vital role in the progression of ARC.
Le texte complet de cet article est disponible en PDF.Keywords : miR-29c-3p, FOS, KCNQ1OT1, Age-related cataract
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Vol 129
Article 110290- septembre 2020 Retour au numéro
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