河北医学2025，Vol.31Issue(5)：705-710,6.DOI:10.3969/j.issn.1006-6233.2025.05.01
灵芝酸A通过调节AMPK/ULK1/mTOR通路对肺癌细胞凋亡和自噬的影响
Ganoderic Acid A Induces Apoptosis and Autophagy in Lung Cancer Cells by Mediating the AMPK/ULK1/mTOR Pathway
摘要
Abstract
Objective:To investigate the effect of ganoderic acid A(GA-A)on apoptosis and autoph-agy in human lung cancer cells by mediating the adenosine 5'-monophosphate-activated protein kinase(AMPK)/unc-51-like autophagy-activating kinase(ULK1)/mammalian target of rapamycin(mTOR)path-way.Methods:The Cell Counting Kit(CCK-8)was used to detect the toxicity of GA-A(0-160 μM)on A549 cells.A549 cells were assigned into control group(Ctrl),low-dose GA-A group(GA-A-L,40 μM),high-dose GA-A group(GA-A-H,80 μM),and high-dose GA-A+AMPK inhibitor group(GA-A-H+compound C).The colony formation experiment was used to detect cell proliferation ability.Flow cytome-try was used to detect apoptosis in A549 cells.MTT method was used to detect cell proliferation;Western blot was used to detect the expression levels of apoptosis,autophagy,and AMPK/ULK1/mTOR pathway-related proteins in A549 cells.Results:Compared with the 0 μM group,the proliferation inhibition rate of A549 cells in the GA-A treatment groups was prominently higher(P<0.05),and the IC50 of GA-A on A549 cells was 81.44 μM.Compared with the control group,the A549 cell survival rate,colony formation rate,Bcl-2 and p62 protein expression,and p-mTOR/mTOR level were prominently lower in the GA-A-L and GA-A-H groups(P<0.05),while the apoptosis rate,number of autophagosomes,Bax protein expression,and LC3B-Ⅱ/Ⅰ,p-AMPK/AMPK,and p-ULK1/ULK1 levels were prominently higher(P<0.05).Compared with the GA-A-H group,the cell survival rate,colony formation rate,Bcl-2 and p62 protein expression,and p-mTOR/mTOR level were prominently higher in the GA-A-H+compound C group(P<0.05),while the apop-tosis rate,number of autophagosomes,Bax protein expression,and LC3B-Ⅱ/Ⅰ,p-AMPK/AMPK,and p-ULK1/ULK1 levels were prominently lower(P<0.05).Conclusion:GA-A may induce apoptosis and auto-phagy in human lung cancer cells and inhibit cell proliferation by regulating the expression of key proteins in the AMPK/ULK1/mTOR pathway.关键词
肺癌细胞/灵芝酸A/腺苷5'-单磷酸活化蛋白激酶/unc-51样自噬激活激酶/哺乳动物雷帕霉素靶蛋白通路Key words
Lung cancer cells/Ganoderic acid A/Adenosine 5'-monophosphate-activated pro-tein kinase/unc-51-like autophagy-activating kinase/mammalian target of rapamycin pathway引用本文复制引用
邓宇新,黄伟,韦思齐,黎恒杰,漆奋强,向敏峰,向水..灵芝酸A通过调节AMPK/ULK1/mTOR通路对肺癌细胞凋亡和自噬的影响[J].河北医学,2025,31(5):705-710,6.基金项目
柳州市科技计划项目,(编号:2024YB0101B010) （编号:2024YB0101B010）
广西壮族自治区卫生健康委自筹经费科研课题,(编号:Z-B20241477) （编号:Z-B20241477）
