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. 2019 Mar 11;11(5):1427–1439. doi: 10.18632/aging.101843

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Copyright © 2019 Ni et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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FOXD2-AS1 regulates the proliferation and migration of glioma cells by miR-185-5p/HMGA2-mediated AKT signaling. (A, B) The influence of miR-185-5p/HMGA2 axis on the proliferation of U251 and U87 cells was analyzed by MTT. (C,D) The effect of miR-185-5p/HMGA2 axis on the migration ability of U251 and U87 cells was analyzed by Transwell migration assay (200×). (E, F) Overexpression of HMGA2 abolished the inhibitory effects of FOXD2-AS1 on cell growth and migration in U251 cells as determined by MTT and migration assay. (G) Effects of the FOXD2-AS1/miR-185-5p/HMGA2 on the mRNA level of PI3K. (H) Effects of the FOXD2-AS1/miR-185-5p/HMGA2 on the levels of PI3K and phospho-Akt (p-AKT) in U251 and U87 cells were examined by Western blot. (I, J) Treatment of SC79 blocked the suppressive effects of FOXD2-AS1 on cell growth and migration in U251 cells. MTT assay and transwell assay were performed with transfected cells that treated with SC79 (5 µg/ml) for 48 h (I) and 24 h (J), respectively. **p < 0.01 vs. Control; ^##p < 0.01 vs. NC; ^&&p < 0.01 vs si-FOXD2-AS1.