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ZFAS1 knockdown inhibits viability and enhances cisplatin cytotoxicity by up‐regulating miR‐432‐5p in glioma cells
Author(s) -
Yang Gongli,
Han Banghua,
Feng Tao
Publication year - 2019
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13286
Subject(s) - gene knockdown , viability assay , glioma , cisplatin , biology , microrna , mtt assay , zinc finger , flow cytometry , cancer research , cell growth , long non coding rna , cell , cytotoxicity , apoptosis , microbiology and biotechnology , chemistry , rna , biochemistry , in vitro , transcription factor , gene , genetics , chemotherapy
Background Long non‐coding RNA (lncRNA) zinc finger antisense 1 (ZFAS1) is a novel vital oncogenic lncRNA that is dysregulated in various types of cancers, including glioma. According to TargetScan prediction, miR‐432‐5p is a target of ZFAS1. Herein, we aimed to determine whether there was a correlation between ZFAS1 and miR‐432‐5p and to explore their roles in glioma. Methods The expression levels of ZFAS1 and microRNA (miR)‐432‐5p in clinical tissues and cell lines were measured using RT‐qPCR. Cell viability was detected using MTT assay. Cell apoptosis was examined using flow cytometry. The association between ZFAS1 and miR‐432‐5p was confirmed using luciferase reporter and RNA pull‐down assays. Results Zinc finger antisense 1 expression was up‐regulated, while miR‐432‐5p expression was down‐regulated in both glioma tissues and cells. Knockdown of ZFAS1 and miR‐432‐5p overexpression inhibited cell viability and enhanced the chemosensitivity of glioma cells to cisplatin. MiR‐432‐5p was a direct target of ZFAS1 in glioma cells. Inhibition of miR‐432‐5p blocked the effects of ZFAS1 knockdown on cell viability and cisplatin sensitivity. Conclusions Knockdown of ZFAS1 inhibited the viability and enhanced cisplatin sensitivity via targeting miR‐432‐5p in glioma cells.