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.
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.