分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Circ_0026134 promotes NSCLC progression by the miR-3619-5p/CHAF1B axis

Liang Ge, Wei Tan, Guangcai Li, Nianjin Gong, Long Zhou

Journal:Thoracic Cancer

IF:3.22

DOI:10.1111/1759-7714.14301

PMID:34985193

Published:2022-01-05

research field:

Abstract

Background Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Circular RNAs (circRNAs) have been implicated in the pathogenesis of NSCLC. In this study, we explored the molecular determinants underlying the oncogenic property of circ_0026134 in NSCLC. Methods The levels of circ_0026134, miR-3619-5p and chromatin assembly factor 1 subunit B axis (CHAF1B) were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell colony formation, migration, invasion and apoptosis were detected by colony formation, Transwell, and flow cytometry assays, respectively. Direct relationships among circ_0026134, miR-3619-5p and CHAF1B were verified by dual-luciferase reporter assays. Results Our results showed that circ_0026134 was highly expressed in NSCLC tissues and cells. Reduced circ_0026134 expression or miR-3619-5p overexpression inhibited NSCLC cell colony formation, migration, invasion, glycolysis and promoted cell apoptosis in vitro. Moreover, circ_0026134 directly targeted miR-3619-5p, and circ_0026134 regulated CHAF1B expression through miR-3619-5p. CHAF1B was a downstream effector of circ_0026134 in affecting NSCLC cell functional behaviors in vitro. Additionally, circ_0026134 silencing weakened tumor growth in vivo. Conclusions Our study identified a novel regulatory mechanism, the circ_0026134/miR-3619-5p/CHAF1B axis, for the oncogenic role of circ_0026134 in NSCLC, highlighting circ_00261345 inhibition as a potential therapeutic method against NSCLC.

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