| 引用本文:王茜1，赵凡尘1，吕祥1，吴建春1，张博1，王媛媛2，方志红1，李雁1.土贝母皂苷甲对肺癌细胞A549的抗肿瘤作用及机制研究[J].世界中医药,2024,(19):. |
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| 土贝母皂苷甲对肺癌细胞A549的抗肿瘤作用及机制研究 |
| Antitumor Effect and Mechanisms of Tubeimoside Ⅰ on A549 Lung Cancer Cells |
| 投稿时间：2023-10-09 |
| DOI：10.3969/j.issn.1673-7202.2024.19.005 |
| 中文关键词: 土贝母皂苷甲 肺癌 肺癌细胞A549 自噬 哺乳动物雷帕霉素信号通路 自噬流 螯合体1 增殖 |
| English Keywords:Tubeimoside Ⅰ Lung cancer A549 lung cancer cells Autophagy Mammalian target of rapamycin signaling pathway Autophagic flow SQSTM1 Proliferation |
| 基金项目:国家自然科学基金面上项目（82174183）——愈创醇靶向mTOR介导的脂质合成增强肺癌干细胞对铁死亡敏感性的机制研究；王羲明名老中医工作室（WLJH2021ZY-GZS006）；未来计划中医药科技发展项目（WL-HBQN-2022018K） |
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| 中文摘要: |
| 目的：探究土贝母皂苷甲（TBMS1）对肺癌细胞A549的抗肿瘤作用及机制。方法：本研究通过细胞增计数剂盒和细胞集落形成试验检测了TBMS1对肺癌细胞A549细胞株细胞活性和增殖能力的影响；通过蛋白质免疫印迹法（WB）实验检测了TBMS1对A549细胞株自噬流的影响，并采用免疫荧光对结果进行了验证；WB实验对自噬核心通路哺乳动物雷帕霉素（mTOR）信号通路进行检测，对其机制进行初步分析。结果：TBMS1能够显著抑制肺癌细胞A549的细胞活力，并且呈现出浓度依赖性的抑制作用；集落形成试验结果显示，TBMS1可以抑制肺癌细胞A549的增殖，减少集落的形成；WB检测结果显示TBMS1增加了微管相关蛋白轻链3(LC3）的形成，诱导了肺癌细胞A549的自噬，并促进了螯合体1（SQSTM1）的降解；TBMS1可能是通过mTOR信号通路促进了细胞自噬。结论：TBMS1通过诱导肺癌细胞A549自噬，促进SQSTM1的降解，抑制了细胞增殖，其机制可能是抑制了mTOR的活性，导致细胞的自噬流受阻。 |
| English Summary: |
| To investigate the antitumor effect and mechanisms of tubeimoside Ⅰ(TBMS1) on A549 lung cancer cells.Methods:The study evaluated the effects of TBMS1 on the viability and proliferation of A549 lung cancer cells using a cell counting kit(CCK) assay and colony formation assay.The influence of TBMS1 on autophagic flux in A549 cells was analyzed through Western blot(WB)，with immunofluorescence used for validation.Additionally，WB was employed to detect the mammalian target of rapamycin(mTOR) signaling pathway，a core autophagy pathway，to preliminarily explore the underlying mechanisms.Results:TBMS1 significantly inhibited the viability of A549 cells in a concentration-dependent manner.The colony formation assay demonstrated that TBMS1 reduced the proliferation of A549 cells and suppressed colony formation.WB results showed that TBMS1 increased the formation of microtubule-associated protein light chain 3(LC3) and induced autophagy in A549 cells，while promoting the degradation of sequestosome 1(SQSTM1).These findings suggest that TBMS1 may promote autophagy via the mTOR signaling pathway.Conclusion:TBMS1 inhibits the proliferation of A549 lung cancer cells by inducing autophagy and promoting the degradation of SQSTM1.Its mechanism likely involves the inhibition of mTOR activity，leading to impaired autophagic flux. |
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