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

Hsa_circRNA_0017620 regulated cell progression of non-small-cell lung cancer via miR-520a-5p/KRT5 axis

Shan Chen, Kelin Hong, Long Zhou, Ruizhi Ran, Jinqi Huang, Yong Zheng, Maohui Xing, Yanli Cai

Journal:JOURNAL OF CLINICAL LABORATORY ANALYSIS

IF:3.12

DOI:10.1002/jcla.24347

PMID:35302673

Published:2022-03-18

research field:蛋白质组学分子生物学胁迫生物学植物科学

Abstract

Background CircRNA is a very important functional RNA that plays an important role in the development and metabolism of cancer. However, the study of circRNA in NSCLC has not been fully elucidated. Methods The expression of hsa_circ_0017620, SFMBT2, miR-520a-5p, and KRT5 was determined using qRT-PCR. KRT5, Twist1, E-cadherin, and Ki67 protein expression were measured with western blot. The positive expression rates of Ki67 and Vimentin were determined by immunohistochemistry assay. 5-Ethynyl-2’-deoxyuridine (EdU), colony formation, and MTT assays were used to assess cell proliferation. Transwell migration and invasion assay were applied to determine cell migration and invasion. Dual-luciferase reporter and RNA immunoprecipitation assays were used to verify the relationship among hsa_circ_0017620, miR-520a-5p, and KRT5. The animal experiment was used to ensure the effects of hsa_circ_0017620 on tumor growth in vivo . Results Hsa_circ_0017620 was upregulated in NSCLC cells and tissues. MiR-520a-5p had been verified to be a target miRNA of hsa_circ_0017620 and KRT5 had been verified to be a target mRNA of miR-520a-5p in NSCLC cells. Knockdown of hsa_circ_0017620 inhibited cell proliferation, migration, and invasion in NSCLC cells, which was reversed by downregulating miR-520a-5p or upregulating KRT5 in NSCLC. Overexpression of hsa_circ_0017620 had opposite effects in NSCLC. Moreover, hsa_circ_0017620 silencing inhibited tumor growth in vivo of NSCLC. Conclusion In this study, we found that hsa_circ_0017620 played an important role in NSCLC progression. Hsa_circ_0017620 regulated cell proliferation, invasion, and migration through targeting miR-520a-5p/KRT5 axis in NSCLC, providing a potential new target for the treatment and diagnosis of NSCLC.

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