Q-F Chen1, J-L Kong, S-C Zou, H Gao, F Wang, S-M Qin, W Wang. 1. Department of Respiratory Medicine, Ward of Pulmonary and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.sriesq@163.com.
Abstract
OBJECTIVE: Non-small cell lung cancer (NSCLC) is the main form of lung cancer, leading to major causes of cancer mortality. It is well known that lncRNAs may be involved in the pathogenesis of cancer, including NSCLC. The aim of this study was to provide a novel therapeutic target of LINC00342 for the therapy of NSCLC. PATIENTS AND METHODS: The expression of LINC00342 and miR-203a-3p was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation was measured using the MTT assay. Colony formation analysis was performed to count the number of colonies. Cell migration and invasion were measured by transwell. Online software DIANA tools were used to predict binding sites of LINC00342 and miR-203a-3p. Luciferase reporter assay was conducted to confirm the interaction between LINC00342 and miR-203a-3p. RESULTS: The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion. LINC00342 regulated the expression of miR-203a-3p by targeting it directly. MiR-203a-3p was down-regulated in NSCLC tissues and cells compared with normal tissues and cells. Furthermore, LINC00342 promoted NSCLC cells proliferation, colony formation, migration, and invasion by depleting the expression of miR-203a-3p. CONCLUSIONS: This work implied that LINC00342 functions in NSCLC acting as an oncogene. Briefly, LINC00342 contributes to NSCLC cells growth and metastasis via targeting miR-203a-3p competitively.
OBJECTIVE:Non-small cell lung cancer (NSCLC) is the main form of lung cancer, leading to major causes of cancer mortality. It is well known that lncRNAs may be involved in the pathogenesis of cancer, including NSCLC. The aim of this study was to provide a novel therapeutic target of LINC00342 for the therapy of NSCLC. PATIENTS AND METHODS: The expression of LINC00342 and miR-203a-3p was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation was measured using the MTT assay. Colony formation analysis was performed to count the number of colonies. Cell migration and invasion were measured by transwell. Online software DIANA tools were used to predict binding sites of LINC00342 and miR-203a-3p. Luciferase reporter assay was conducted to confirm the interaction between LINC00342 and miR-203a-3p. RESULTS: The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion. LINC00342 regulated the expression of miR-203a-3p by targeting it directly. MiR-203a-3p was down-regulated in NSCLC tissues and cells compared with normal tissues and cells. Furthermore, LINC00342 promoted NSCLC cells proliferation, colony formation, migration, and invasion by depleting the expression of miR-203a-3p. CONCLUSIONS: This work implied that LINC00342 functions in NSCLC acting as an oncogene. Briefly, LINC00342 contributes to NSCLC cells growth and metastasis via targeting miR-203a-3p competitively.
Authors: Wen Deng; Gongxian Wang; Huanhuan Deng; Yan Yan; Ke Zhu; Ru Chen; Xiaoqiang Liu; Luyao Chen; Tao Zeng; Bin Fu Journal: Int J Gen Med Date: 2021-12-14