Circ_0000877 accelerates proliferation and immune escape of non‐small cell lung cancer cells by regulating microRNA‐637/E2F2 axis

Author:

Chen Ting'an1,Li Zhengdong2,Chen Junzhu1,Xu Zhe3ORCID

Affiliation:

1. Department of Pathology Guangyuan Central Hospital Guangyuan Sichuan China

2. Precision Medical Centre Guangyuan Central Hospital Guangyuan Sichuan China

3. Guangyuan Central Hospital Guangyuan Sichuan China

Abstract

AbstractBackgroundRecently, circular RNA (circRNA) has become a vital targeted therapy gene for non‐small‐cell lung cancer (NSCLC) cells. CircRNA_0000877 (Circ_0000877) has been researched in diffuse large B‐cell lymphoma (DLBCL). However, whether circ_0000877 regulated NSCLC cell progression is still poorly investigated. The research attempted to investigate the influence of circ_0000877 in NSCLC.MethodsCirc_0000877 levels in NSCLC tissues and cell lines were determined applying RT‐qPCR. Cell functions were evaluated by CCK‐8, EdU, flow cytometry, ELISA, and western blot. Gene interactions were predicted by Cirular RNA interactome database and Target Scan website and certified by dual‐luciferase reporter, RIP, and RNA pull‐down assays. Finally, mice experimental model was established to explore the effects of circ_0000877 on tumor growth in vivo.ResultsThe elevated trend of circ_0000877 expression was discovered in NSCLC tissues compared to para‐carcinoma tissues. The clinicopathological data uncovered that up‐regulated circ_0000877 was linked to tumor size, differentiation, and TNM stages of NSCLC patients. Knockdown of circ_0000877 inhibited the proliferation, triggered apoptosis, and prohibited immune escape in NSCLC cells. It was certified that miR‐637 was directly interacted with circ_0000877 and targeted by E2F2. Overexpressed E2F2 strongly overturned the functions of circ_0000877 knockdown in NSCLC cells. Mice experimental data demonstrated that circ_0000877 knockdown suppressed tumor growth in vivo.ConclusionThe research demonstrated that circ_0000877 exhibited the promotive effect on NSCLC cells proliferation and immune escape by regulating miR‐637/E2F2 axis.

Publisher

Wiley

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