MiR-128-3p Regulates Proliferation, Migration and Apoptosis of Glioblastoma Multiforme by Targeting HOXA5

• Main Authors: YANG Jipeng, QIU Xiang, LI Chen, YANG Jiankai, LIU Hongjiang, JIAO Baohua
• Format: Article
• Language: zho
• Published: Magazine House of Cancer Research on Prevention and Treatment 2021-01-01
• Series: Zhongliu Fangzhi Yanjiu
• Subjects: glioblastoma multiforme; hoxa5; mir-128-3p; cell proliferation; migration; apoptosis
• Online Access: http://html.rhhz.net/ZLFZYJ/html/8578.2021.20.0595.htm
• ISSN: 1000-8578; 1000-8578

Objective To investigate the reasons of HOXA5 overexpression in GBM and the molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of glioblastoma multiforme. Methods After increasing and decreasing miR-128-3p expression in U87 cell lines by lentivirus transfection, the changes of HOXA5 expression were detected by Western blot, to explore the correlation between miR-128-3p and HOXA5 in GBM. The dual-luciferase reporter tests were performed to detect the target interaction of miR-128-3p with HOXA5. Through CCK-8 test, Transwell test, flow cytometric assay and tumor cell xenograft in nude mice, we verified molecular mechanism of miR-128-3p regulating the proliferation, invasion and apoptosis of GBM in vitro and in vivo. Results The expression level of HOXA5 was decreased in U87 cell line after miR-128-3p upregulation. In addition, the expression level of HOXA5 was increased in U87 cell line after miR-128-3p downregulation (P < 0.05). The expression level of HOXA5 was correlated negatively with the expression of miR-128-3p in U87 cell lines. MiR-128-3p targetedly interacted with 3'UTR of HOXA5 and inhibited the expression of HOXA5. The proliferation, invasion and anti-apoptosis of U87 cells were significantly decreased in the miR-128-3p+control group. Conclusion MiR-128-3p regulates negatively the proliferation, invasion and anti-apoptosis of GBM cells by targeting HOXA5. The overexpression of HOXA5 is induced by downregulation of miR-128-3p in GBM.