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环状 RNA circFARSA 通过海绵吸附 miR-15a-5p 来升高 B7H3 促进非小细胞肺癌的肿瘤发生。

Circular RNA circFARSA promotes the tumorigenesis of non-small cell lung cancer by elevating B7H3 via sponging miR-15a-5p.

机构信息

Department of Pulmonary and Critical Care Medicine, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.

Vascular Disease Research Center, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China.

出版信息

Cell Cycle. 2022 Dec;21(24):2575-2589. doi: 10.1080/15384101.2022.2105087. Epub 2022 Aug 3.

DOI:10.1080/15384101.2022.2105087
PMID:35920698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9704387/
Abstract

Non-small cell lung cancer (NSCLC) is currently one of the malignant tumors with the highest incidence and mortality rate in China. Circular RNA hsa_circ_0000896 (circFARSA) has been reported as being an oncogene and a potential biomarker for NSCL. However, the functional role and action mechanism of circFARSA in NSCLC progression have not been fully elucidated. The present study demonstrated that circFRASA was upregulated in NSCLC tissues and cell lines, and its expression was positively correlated with poor prognosis of patients with NSCLC. Further experiments revealed that circFARSA knockdown inhibited cell proliferation, migration, and invasion experiments, but overexpression of circFARSA exhibited opposite results. Mechanistically, circFARSA facilitated the malignant phenotype of NSCLC cells by enhancing B7H3 expression through sponging miR-15a-5p. experiments, knockdown of circFARSA restricted tumor growth and metastasis. In conclusion, circFARSA served as a sponge of miR-15a-5p to promote tumorigenesis and development of NSCLC by upregulation of B7H3 expression, which provided evidence of circFARSA maybe act as a novel therapeutic target for NSCLC.

摘要

非小细胞肺癌(NSCLC)是目前中国发病率和死亡率最高的恶性肿瘤之一。环状 RNA hsa_circ_0000896(circFARSA)已被报道为一种癌基因和 NSCLC 的潜在生物标志物。然而,circFARSA 在 NSCLC 进展中的功能作用和作用机制尚未完全阐明。本研究表明,circFRASA 在 NSCLC 组织和细胞系中上调,其表达与 NSCLC 患者的不良预后呈正相关。进一步的实验表明,circFARSA 敲低抑制细胞增殖、迁移和侵袭实验,但过表达 circFARSA 则表现出相反的结果。机制上,circFARSA 通过海绵吸附 miR-15a-5p 增强 B7H3 表达,促进 NSCLC 细胞的恶性表型。实验,circFARSA 的敲低限制了肿瘤的生长和转移。总之,circFARSA 通过上调 B7H3 表达作为 miR-15a-5p 的海绵促进 NSCLC 的发生和发展,为 circFARSA 可能作为 NSCLC 的一种新的治疗靶点提供了证据。

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