陕西医学杂志2024，Vol.53Issue(7)：879-883,5.DOI:10.3969/j.issn.1000-7377.2024.07.003
莫诺苯宗对肺腺癌细胞自噬和凋亡的分子机制研究
Molecular mechanism of monobenzone on autophagy and apoptosis in lung adenocarcinoma cells
摘要
Abstract
Objective:To explore the effects of monobenzone and natural killer cell activating receptor gene(KLRC3)on apoptosis and autophagy of lung adenocarcinoma(LUAD)cells,and to provide a theoretical basis for the treatment of LU AD.Methods:The LU AD cells were treated with different concentrations of monobenzone,and the effect of monobenzone on the viability of LUAD cells was detected by CCK-8 method.Subsequently,the LU AD cells were treated with 80 μmol/L monobenzone,50 nmol/L KLRC3 interference plasmid(si-KLRC3),100 nmol/L autophagy inhibitor 3-methyladenine(3-MA),and 1.5 μg/ml KLRC3 overexpression vector(pcDNA-KLRC3).Then,flow cytometry and Western blot were used to detect apoptosis and the expression of apoptosis-related proteins and autophagy-related proteins.Results:The results showed that when the concentration of monobenzone was greater than 20 μmol/L,it could effectively reduce the viability of LUAD cells and promote the apoptosis and autophagy of LUAD cells in a dose-dependent manner(all P＜0.05).The expression of KLRC3 was downregulated in LUAD cells.Knockdown of KLRC3 attenuated the promotion of monobenzone on autophagy and apoptosis in LUAD cells(all P＜0.05).In addition,overexpression of KLRC3 also promoted the apoptosis and autophagy of LUAD cells,while the promotion of KLRC3 and monobenzone on the apoptosis and autophagy of LUAD cells could be offset by 3-MA(all P＜0.05).Conclusion:This study shows that monobenzone may induce autophagy by promoting the ex-pression of KLRC3 and promote the apoptosis of LUAD cells.关键词
肺腺癌/莫诺苯宗/自然杀伤细胞激活受体基因/自噬/细胞凋亡/细胞活力Key words
Lung adenocarcinoma/Monobenzone/Natural killer cell activating receptor gene/Autophagy/Ap-optosis/Cell viability分类
医药卫生引用本文复制引用
刘亚,庞亚梅,李宏,阳甜,宁谦,任徽..莫诺苯宗对肺腺癌细胞自噬和凋亡的分子机制研究[J].陕西医学杂志,2024,53(7):879-883,5.基金项目
陕西省自然科学基础研究计划项目(2018JQ8044) （2018JQ8044）
