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

CircRNA CDR1as knockdown inhibits progression of non-small-cell lung cancer by regulating miR-219a-5p/SOX5 axis

Yaming Li, Jinzhao Zhang, Shuang Pan, Jing Zhou, Xin Diao, Song Liu

Journal:Thoracic Cancer

IF:2.61

DOI:10.1111/1759-7714.13274

PMID:31917898

Published:2020-01-09

research field:肿瘤学细胞生物学表观遗传学

Abstract

Background Circular RNAs (circRNAs) participate in the development of human cancers by regulating multiple cell processes. CircRNA antisense to the cerebellar degeneration-related protein 1 transcript (circCDR1as) expression is dysregulated in many cancers, including non-small-cell lung cancer (NSCLC). However, the mechanism by which circCDR1as mediates the development of NSCLC remains unknown. Methods A total of 30 paired cancer and normal tissues were collected from patients with NSCLC. The expression levels of circCDR1as, microRNA (miR)-219a-5p and Sex determining region Y-box protein 5 (SOX5) were measured in tissues or cells by quantitative real-time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, colony formation, flow cytometry and transwell assays, respectively. The target relationship between miR-219a-5p and circCDR1as or SOX5 was validated by dual-luciferase reporter assay. Results CircCDR1as expression was elevated in NSCLC tissues and cells in comparison to the matched controls. Interference of circCDR1as led to obvious inhibition of cell viability, migration and invasion and increase of apoptosis in NSCLC cells. MiR-219a-5p acted as a target of circCDR1as and miR-219a-5p downregulation attenuated the regulatory effect of circCDR1as silencing on NSCLC progression. Moreover, miR-219a-5p targeted SOX5 to repress the progression of NSCLC in vitro. Besides, circCDR1as knockdown reduced the expression of SOX5 by increasing miR-219a-5p level. Conclusion Knockdown of circCDR1as inhibited the progression of NSCLC by decreasing cell viability, migration and invasion and increasing apoptosis by upregulating miR-219a-5p and downregulating SOX5.

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