| 朱文忠,谭路露,马田田,姚 潇,高金波.基于PI3K/AKT/mTOR信号通路探讨二甲双胍对结肠癌HCT116细胞的作用[J].,2022,(3):413-417 |
| 基于PI3K/AKT/mTOR信号通路探讨二甲双胍对结肠癌HCT116细胞的作用 |
| Explore the Effect of Metformin on Colon Cancer HCT116 Cells Based on PI3K-AKT-mTOR Signaling Pathway |
| 投稿时间：2021-06-28 修订日期：2021-07-23 |
| DOI：10.13241/j.cnki.pmb.2022.03.003 |
| 中文关键词: 二甲双胍 结肠癌 增殖 凋亡 磷脂酰肌醇3激酶/蛋白激酶 B/哺乳动物雷帕霉素靶蛋白 |
| 英文关键词: Metformin Colon cancer Proliferation Apoptosis Phosphatidylinositol 3 kinase/protein kinase B/mammalian target of rapamycin |
| 基金项目:湖北省自然科学基金项目（2015CFB710） |
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| 中文摘要: |
| 摘要 目的：研究二甲双胍通过磷脂酰肌醇3激酶（PI3K）/蛋白激酶 B(Akt)/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路对结肠癌HCT116 细胞的作用。方法：体外培养结肠癌HCT116细胞，分别加入二甲双胍(20，40，80 μmol/L)处理HCT116细胞48 h，另设对照组。MTT法检测各组细胞增殖能力。Transwell实验检测各组细胞侵袭能力的变化。Annexin-FITC/PI 双染法分别检测各组处理48 h后细胞凋亡情况。免疫印迹法检测48 h后PI3K/Akt/mTOR通路蛋白表达水平。结果：相比于对照组，二甲双胍20，40，80 μmol/L各处理组对HCT116细胞的增殖具有明显的抑制作用，且呈浓度依赖效应，差异具有统计学意义(P＜0.05)。与对照组比较，二甲双胍20，40，80 μmol/L各处理组细胞凋亡率明显较高，且呈浓度依赖效应，差异具有统计学意义(P＜0.05)。相比于对照组，二甲双胍20，40，80 μmol/L各处理组HCT116细胞侵袭能力明显减弱，且呈浓度依赖效应，差异具有统计学意义(P <0.05)。与对照组比较，二甲双胍20，40，80 μmol/L各处理组Bax蛋白表达水平明显升高，而Bcl-2、p-Akt及p-mTOR蛋白表达水平明显降低，且呈浓度依赖效应，差异具有统计学意义(P＜0.05)。结论：二甲双胍在体外可抑制人结肠癌HCT-116细胞的增殖，促进其凋亡，抑制其侵袭能力，其抗肿瘤机制可能与抑制PI3K/Akt/mTOR 信号通路激活相关。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effect of metformin on colon cancer HCT-116 cells through the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway. Methods: Colon cancer HCT116 cells were cultured in vitro, and metformin (20, 40, 80 μmol/L) was added to treat HCT-116 cells for 48 hours, and a control group was set up. MTT method was used to detect the proliferation ability of cells in each group. Transwell experiment detects the changes of cell invasion ability in each group. The Annexin-FITC/PI double staining method was used to detect the apoptosis of each group at 48 hours after treatment.Western blotting was used to detect the protein expression level of PI3K/Akt/mTOR pathway after 48 hours. Results: Compared with the control group, the metformin 20, 40, and 80 μmol/L treatment groups had a significant inhibitory effect on the proliferation of HCT-116 cells, and showed concentration-dependent effect, with statistical significance(P＜0.05). Compared with the control group, the apoptotic rate of the metformin 20, 40, 80 μmol/L treatment groups were significantly higher, and showed concentration-dependent effect, with statistical significance(P＜0.05). Compared with the control group, the invasion ability of HCT116 cells in metformin 20, 40 and 80 μmol/L treatment groups was significantly decreased, and showed concentration-dependent effect, with statistical significance(P＜0.05). Compared with the control group, the expression levels of Bax protein in metformin 20, 40 and 80 μmol/L treatment groups were significantly increased, while the expression levels of Bcl-2, p-Akt and p-mTOR protein were significantly decreased, and showed concentration-dependent effect, with statistical significance(P＜0.05). Conclusion: Metformin can inhibit the proliferation, apoptosis and invasion of human colon cancer HCT-116 cells in vitro, and its anti-tumor mechanism may be related to the inhibition of PI3K/Akt/mTOR signaling pathway activation. |
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