LncRNA GAS5 modulates the progression of non-small cell lung cancer through repressing miR-221-3p and up-regulating IRF2

Diagnostic Pathology

Haiyun Zhang¹  Feifan Xu¹  Jingjing Ren¹  Shengyan Qu¹  Juan Ma¹  Jing Da²  Haiyan Miao³  Huan Zhao⁴ 

[1] Department of Clinical Laboratory, The Sixth People’s Hospital of Nantong;Department of Gastroenterology, The Sixth People’s Hospital of Nantong;Department of General Surgery, The Sixth People’s Hospital of Nantong;Department of Respiration, The Sixth People’s Hospital of Nantong;

关键词: NSCLC;    lncRNA GAS5;    miR-221-3p;    IRF2;   

DOI  :  10.1186/s13000-021-01108-0

来源: DOAJ

【 摘 要 】

Abstract Background Long non-coding RNA growth arrest specific 5 (GAS5) is a regulator in non-small cell lung cancer (NSCLC) progression. Nonetheless, the mechanism by which GAS5 exerts its biological function in NSCLC cells remains unclear. Methods GAS5, miR-221-3p relative expression levels in NSCLC tissues and cells were examined by qPCR. After gain-of-function and loss-of-function models were established, the viability of H1299 and A549 cells were examined by CCK-8 and EdU assays. Cell migration and invasion were examined by the Transwell experiment. The binding sequence of GAS5 for miR-221-3p was confirmed by the dual-luciferase reporter gene experiment. The regulatory function of GAS5 and miR-221-3p on IRF2 was investigated by Western blot. Results GAS5 expression was down-modulated in NSCLC tissues and cell lines. GAS5 overexpression restrained the proliferation, migration and invasion of NSCLC cells, while miR-221-3p, which was targeted and negatively modulated by GAS5, worked oppositely. Restoration of miR-221-3p markedly reversed the effects of GAS5 on NSCLC cells. Additionally, GAS5 increased IRF2 expression in NSCLC cells by repressing miR-221-3p. Conclusions GAS5 blocks the progression of NSCLC partly via increasing IRF2 expression level via repressing miR-221-3p.

【 授权许可】

Unknown