| First Author | Liu M | Year | 2016 |
| Journal | Gene | Volume | 576 |
| Issue | 1 Pt 2 | Pages | 304-11 |
| PubMed ID | 26484393 | Mgi Jnum | J:229406 |
| Mgi Id | MGI:5751936 | Doi | 10.1016/j.gene.2015.10.038 |
| Citation | Liu M, et al. (2016) MicroRNA-29c overexpression inhibits proliferation and promotes apoptosis and differentiation in P19 embryonal carcinoma cells. Gene 576(1 Pt 2):304-11 |
| abstractText | Compared to healthy controls, microRNA-29c (miR-29c) is highly expressed in the heart during progression towards ventricular septal defect. However, studies on miR-29c function in heart development are scarce. We investigated the role of miR-29c in P19 cell proliferation, apoptosis, and differentiation and the underlying mechanisms. We evaluated proliferation and cell cycle progression, detected morphological changes; apoptosis rate; BAX, BCL2, GATA binding protein 4 (GATA4), cardiac troponin T (cTnT), and myocyte enhancer factor 2C (MEF2C) expression; and caspase-3, -8, and -9 activity in miR-29c-overexpressing P19 cells, and investigated whether WNT4 was a miR-29c target. MiR-29c-overexpressing cells had decreased proliferation, increased G1 cells, and significantly higher apoptotic rate than the controls. Expression of the apoptosis-related BAX and BCL2 genes and caspase-3, -8, and -9 activity were significantly increased in miR-29c-overexpressing cells. Expression of the cardiac-specific markers GATA4, cTnT, and MEF2C revealed promoted differentiation in miR-29c-overexpressing cells compared to the controls. Luciferase assay confirmed that WNT4 is a miR-29c target. Wnt4 and beta-catenin expression was decreased in miR-29c-overexpressing cells. MiR-29c inhibits P19 cell proliferation and promotes apoptosis and differentiation, possibly by suppressing Wnt4 signaling, whose deregulation contributes to congenital heart disease development. |
