LncRNA LUCAT1通过调节miR-493-5p/RAC1轴对非小细胞肺癌细胞增殖凋亡和侵袭的影响

doi:10.3969/j.issn.1006-6233.2022.10.06

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Abstract Objective: To elucidate the underlying mechanism of the long non-coding RNA (lncRNA) lung cancer associated transcript 1 (LUCAT1) on non-small cell lung cancer (NSCLC). Methods: RT-qPCR and Western blot were used to determine gene and protein expression levels.Dual-luciferase reporter gene (DLRG) was used to verify the relationship between miR-493-5p and LUCAT1 or RAC1.CCK-8,colony formation,flow cytometry and Transwell were applied to evaluate the cell biological behaviors.In addition,the biological function of LUCAT1 in NSCLC was investigated by tumor xenograft experiments. Results: The expression of LUCAT1 and RAC1 mRNA was up-regulated in NSCLC tissues and cell lines,and the expression of miR-493-5p was down-regulated (P<0.05); moreover,in NSCLC,it was observed that LUCAT1 was negatively correlated with miR-493-5p and positively correlated with RAC1 mRNA,and miR-493-5p was negatively correlated with RAC1 mRNA (P<0.05).DLRG confirmed the interaction between miR-493-5p and LUCAT1 or RAC1 (P<0.05).Silencing LUCAT1 could significantly up-regulate the level of miR-493-5p and down-regulate the level of RAC1 (P<0.05).Silencing LUCAT1 significantly attenuated cell proliferative viability,decreased invasion abilities,and promoted cell apoptosis (P<0.05).In addition,inhibition of miR-493-5p or overexpression of RAC1 could partially reverse the effects of LUCAT1 silencing on NSCLC cells (P<0.05).In vivo xenograft tumor experiments confirmed that silencing LUCAT1 significantly inhibited the growth of NSCLC tumors in vivo (P<0.05). Conclusion: LUCAT1 silencing inhibits NSCLC tumorigenesis by regulating the miR-493-5p/RAC1 axis.

Key words： LUCAT1 miR-493-5p RAC1 Non-small cell lung cancer

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.10.06 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I10/1614

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