组蛋白脱乙酰基酶5
癌症研究
转染
小RNA
细胞凋亡
生物
组蛋白脱乙酰基酶
细胞生物学
细胞培养
组蛋白
生物化学
基因
遗传学
作者
Dongxian Peng,Tingting Wu,Junxia Wang,Jie Huang,Ling Zheng,Pingping Wang,Junpeng Li,Lin Wu,Min Luo
标识
DOI:10.1016/j.cbi.2021.109780
摘要
microRNA (miR)-based therapeutic reference has been established and expanded in the treatment of cancers. For this reason, we explored how miR-671-5p regulated tumorigenicity of ovarian cancer (OC) through regulating histone deacetylase 5 (HDAC5) and hypoxia-inducible factor-1α (HIF-1α).miR-671-5p, HDAC5 and HIF-1α expression levels were determined in OC clinical tissues. The OC cell line H8910 was screened and transfected with the vectors that altered miR-671-5p, HDAC5 and HIF-1α levels. Finally, the proliferation, migration, invasion and apoptosis of the transfected H8910 cells were determined and the role of miR-671-5p and HDAC5 in vivo tumor growth was further discussed.Low expression miR-671-5p and high expression HDAC5 and HIF-1α levels were tested in OC tissues. Up-regulating miR-671-5p or down-regulating HDAC5 or HIF-1α suppressed proliferation, migration, invasion and augmented apoptosis of H8910 cells while silenced miR-671-5p or enhanced HDAC5 caused the opposite consequences. Overexpression of HDAC5 reduced while depletion of HDAC5 enhanced the influence of up-regulated miR-671-5p on OC cell growth. In animal models, suppressing miR-671-5p or promoting HDAC5 encouraged OC tumor growth.A summary delineates that miR-671-5p reduces tumorigenicity of OC via suppressing HDAC5 and HIF-1α expression levels.
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