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

基因敲除 小RNA 免疫系统 癌症研究 体内 流式细胞术 细胞生长 报告基因 肺癌 生物 细胞凋亡 化学 分子生物学 基因表达 免疫学 基因 生物化学 肿瘤科 医学 生物技术
作者
Ting'an Chen,Zhengdong Li,Jun-zhu Chen,Zhe Xu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:39 (5): 2980-2992 被引量:3
标识
DOI:10.1002/tox.24172
摘要

Abstract Background Recently, 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. Methods Circ_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. Results The 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. Conclusion The research demonstrated that circ_0000877 exhibited the promotive effect on NSCLC cells proliferation and immune escape by regulating miR‐637/E2F2 axis.
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