[1]刘 亚,庞亚梅,李 宏,等.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,(7):879-883.[doi:DOI:10.3969/j.issn.1000-7377.2024.07.003]
　LIU Ya,PANG Yamei,LI Hong,et al.Molecular mechanism of monobenzone on autophagy and apoptosis in lung adenocarcinoma cells[J].,2024,(7):879-883.[doi:DOI:10.3969/j.issn.1000-7377.2024.07.003]
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莫诺苯宗对肺腺癌细胞自噬和凋亡的分子机制研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
期数:
2024年7期
页码:
879-883
栏目:
基础研究
出版日期:
2024-07-05

文章信息/Info

Title:
Molecular mechanism of monobenzone on autophagy and apoptosis in lung adenocarcinoma cells
作者:
刘 亚; 庞亚梅; 李 宏; 阳 甜; 宁 谦; 任 徽
(西安交通大学第一附属医院呼吸与危重症医学科,陕西 西安 710061)
Author(s):
LIU Ya; PANG Yamei; LI Hong; YANG Tian; NING Qian; REN Hui
(Department of Respiratory and Critical Care Medicine,First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China)
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
Keywords:
Lung adenocarcinoma;  Monobenzone;  Natural killer cell activating receptor gene;  Autophagy;  Apoptosis;  Cell viability
分类号:
R -33
DOI:
DOI:10.3969/j.issn.1000-7377.2024.07.003
文献标志码:
A
摘要:
目的:探究莫诺苯宗和自然杀伤细胞激活受体基因(KLRC3)对肺腺癌(LUAD)细胞凋亡和自噬的影响,为LUAD的治疗提供理论基础。方法:分别使用不同浓度莫诺苯宗处理LUAD细胞,并采用CCK-8法检测莫诺苯宗对LUAD细胞活力的影响; 随后,使用80 μmol/L的莫诺苯宗、50 nmol/L 的KLRC3干扰质粒(si-KLRC3)、和100 nmol/L自噬抑制剂3-甲基腺嘌呤(3-MA)1.5 μg/ml KLRC3过表达载体(pcDNA-KLRC3)处理细胞后采用流式细胞术和Western blotting检测细胞凋亡以及凋亡相关蛋白和自噬相关蛋白的表达量。结果:莫诺苯宗浓度大于20 μmol/L时可有效减弱LUAD细胞活力,且以剂量依赖性地促进了LUAD细胞的凋亡和自噬(均P<0.05)。KLRC3在LUAD细胞中低表达,干扰KLRC3减弱了莫诺苯宗对LUAD细胞自噬和凋亡的促进作用,比较差异有统计学意义(均P<0.05)。此外,过表达KLRC3也促进了LUAD细胞的凋亡和自噬,而KLRC3和莫诺苯宗对LUAD细胞凋亡和自噬的促进作用均可被3-MA所抵消,比较差异有统计学意义(均P<0.05)。结论:莫诺苯宗可能通过促进KLRC3的表达诱导自噬进而促进LUAD细胞的凋亡。
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 LUAD. Methods:The LUAD 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 LUAD 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 expression of KLRC3 and promote the apoptosis of LUAD cells.

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备注/Memo

备注/Memo:
基金项目:陕西省自然科学基础研究计划项目(2018JQ8044)
更新日期/Last Update: 2024-07-04