白藜芦醇通过抑制Akt/mTOR信号通路活性促进肺癌细胞自噬发挥抗肿瘤效应的研究<sup>★</sup>

doi:10.3969/j.issn.2095-1264.2023.02.08

首页 > 过刊浏览>2023年第2期 >181-186. DOI:10.3969/j.issn.2095-1264.2023.02.08

白藜芦醇通过抑制Akt/mTOR信号通路活性促进肺癌细胞自噬发挥抗肿瘤效应的研究★
DOI:
                        10.3969/j.issn.2095-1264.2023.02.08
                    
作者:
                        
                        
                    
作者单位:广元市中心医院 呼吸内科，四川 广元，628017
作者简介:闫菊，女，硕士，主管护师，研究方向：肺癌生物学。
通讯作者:翟飞，男，硕士，主治医师，研究方向：肺癌生物学。
中图分类号:R734.2
基金项目:★四川省卫生健康委员会科研课题（17PJ265）。

Antitumor effects of resveratrol by inhibiting the Akt/mTOR signaling pathway activity and promoting the autophagy of lung cancer cells ^★

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Affiliation:

Department of Respiratory Medicine, Guangyuan Central Hospital, Guangyuan, 628017, Sichuan, China

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摘要:

目的探讨白藜芦醇对肺癌细胞生长活性的抑制效应及可能的机制。方法稳定培养肺癌细胞系H292，分别加入含10、20、40 μmol·L^-1白藜芦醇的培养基进行干预，采用CCK-8、流式细胞术、细胞集落形成实验检测白芦藜醇对H292细胞生长活性的影响，采用免疫荧光、Western blotting检测白藜芦醇对细胞Akt/mTOR信号通路相关蛋白的影响。结果（1） CCK-8检测结果显示，白藜芦醇对H292细胞增殖有明显抑制作用（P<0.05），且呈时间和剂量依赖性，同时对H292细胞周期有明显影响，能阻滞细胞周期于G₂/M期。（2）白藜芦醇可明显抑制H292细胞集落形成（P<0.05），并呈剂量依赖性。（3） Western blotting检测结果显示，白藜芦醇以剂量依赖的方式诱导H292细胞中LC3-II的累积。免疫荧光检测发现，白藜芦醇可诱导细胞核和线粒体中GFP-LC3显著增加。（4）自噬抑制剂3-MA能有效减弱白藜芦醇对H292细胞活力的抑制作用，溶酶体酸化抑制剂Bafilomycin A1则可促进白藜芦醇导致的LC3-II累积。（5）白藜芦醇可下调H292细胞中p-Akt、p-P70S6K、p-mTOR蛋白的表达（P<0.05），而对Akt、P70S6K、mTOR蛋白的表达无明显影响（P>0.05）。结论白藜芦醇可通过抑制Akt/mTOR信号通路抑制肺癌细胞的增殖。

Abstract:

Objective To investigate the effect of resveratrol on the growth activity of lung cancer cells and its possible mechanism.Methods The lung cancer cell line H292 was stably cultured, and the medium containing resveratrol of different concentrations was added for intervention. CCK-8 test, flow cytometry and cell colony formation test were used to detect the effects of resveratrol on the growth activity of H292 cells. Immunofluorescence and Western blotting were used to detect the effects of resveratrol on the expressions of Akt/mTOR signaling pathway-related proteins in H292 cells.Results (1) CCK-8 results showed that resveratrol significantly inhibited the proliferation of H292 cells (P<0.05) in a time- and dose-dependent manner. At the same time, resveratrol had a significant effect on the cell cycle of H292, which could arrest the cell cycle at G₂/M phase. (2) Resveratrol significantly inhibited the colony formation of H292 cells in a dose-dependent manner (P<0.05). (3) Western blotting showed that resveratrol induced the accumulation of LC3-II in H292 cells in a dose-dependent manner. Immunofluorescence assay showed that resveratrol induced a significant increase of GFP-LC3 in the nucleus and mitochondria. (4) Autophagy inhibitor 3-MA effectively weakened the inhibitory effect of resveratrol on the viability of H292 cells. Lysosomal acidification inhibitor Bafilomycin A1 promoted the accumulation of LC3-II which was induced by resveratrol. (5) Resveratrol down-regulated the expressions of p-Akt, p-P70S6K and p-mTOR proteins in H292 cells (P<0.05), but had no significant effects on the expressions of Akt, P70S6K and mTOR proteins (P>0.05).Conclusion Resveratrol can inhibit the proliferation of lung cancer cells by suppressing the Akt/mTOR signal pathway activity.