| 陈西,欧阳紫婷,罗岚,沈艳,宁东红,梁煦.当归酮通过PI3K/Akt/mTOR信号通路抑制子宫内膜癌细胞RL95-2自噬.[J].中南医学科学杂志.,2025,(2):217-220. |
| 当归酮通过PI3K/Akt/mTOR信号通路抑制子宫内膜癌细胞RL95-2自噬 |
| Angelicone inhibits the autophagy of endometrial cancer cells RL95-2 through PI3K/Akt/mTOR signaling pathway |
| 投稿时间：2023-09-22 修订日期：2024-11-28 |
| DOI：10.15972/j.cnki.43-1509/r.2025.02.006 |
| 中文关键词: 当归酮 PI3K/Akt/mTOR 子宫内膜癌 自噬 RL95-2细胞 [ |
| 英文关键词:angelicone PI3K/Akt/mTOR endometrial cancer autophagy RL95-2 cells |
| 基金项目:湖南省中医药科研计划项目(2021316) |
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| 中文摘要: |
| 目的探讨当归酮抑制子宫内膜癌细胞RL95-2自噬的作用机制。 方法设置不同浓度当归酮(0、2.5、5.0、10.0、20.0 μmol/L)作用于RL95-2细胞,筛选最佳作用浓度。细胞实验分为对照组(DMSO培养24 h)、当归酮组(20.0 μmol/L当归酮原液培养24 h)、当归酮＋胰岛素样生长因子-1(IGF-1)组[20.0 μmol/L当归酮和磷脂酰肌醇3激酶(PI3K)激活剂IGF-1共同培养24 h]。采用透射电子显微镜观察自噬体的形成,免疫荧光显微镜检测各组微管相关蛋白1轻链3(LC3)的表达水平。Western blotting检测各组信号通路关键蛋白PI3K-p85、蛋白质丝氨酸/苏氨酸激酶(Akt)、哺乳动物雷帕霉素靶蛋白(mTOR)及其磷酸化蛋白水平。 结果当归酮最佳作用浓度为20.0 μmol/L。随着当归酮处理时间的递增,细胞内自噬体数量及LC3针点数逐渐增加(P＜0.05),磷酸化(p)-Akt、p-mTOR、PI3K-p85表达水平逐渐降低(P＜0.05)。与对照组相比,当归酮组细胞自噬体数量增加,LC3蛋白表达水平升高(P＜0.05)；与当归酮组相比,当归酮+IGF-1组细胞自噬体数量减少,LC3蛋白表达水平降低(P＜0.05)。 结论当归酮可能通过PI3K/Akt/mTOR信号通路抑制人子宫内膜癌细胞RL95-2的自噬。 |
| 英文摘要: |
| AimTo investigate the mechanism of angelicone in inhibiting autophagy of endometrial cancer cell RL95-2. MethodsDifferent concentrations of angelicone (0,2.5,5.0,10.0,20.0 μmol/L) were applied to RL95-2 cells to screen for the optimal concentration. The cells were divided into the control group (DMSO treated for 24 hours), the angelicone group (20.0 μmol/L angelicone stock solution treated for 24 h), and the angelicone +insulin-like growth factor-1 (IGF-1) group [(20.0 μmol/L angelicone and phosphoinositide 3-kinase (PI3K) activator IGF-1 co-treated for 24 h). Transmission electron microscopy was used to observe the formation of autophagosomes, and immunofluorescence microscopy was used to detect the expression levels of microtubule associated protein 1 light chain 3 (LC3) in each group. Western blotting was used to detect the levels of key proteins in various signaling pathways, including PI3K-p85, protein serine/threonine kinase (Akt), mammalian target of rapamycin (mTOR), and their phosphorylated proteins. ResultsThe optimal concentration for screening angelicone was 20.0 μmol/L. With the increasing treatment time of angelicone, the number of autophagosomes and LC3 needle points in cells gradually were increased (P＜0.05), while the expression levels of phosphorylated (p)-Akt, p-mTOR, and PI3K-p85 in cells gradually were decreased (P＜0.05). Compared with the control group, the angelicone group showed an increase in number of autophagosomes and elevated expression levels of LC3 protein (P＜0.05). Compared with the angelicone group, the angelicone+IGF-1 group showed a decrease in number of autophagosomes and a decrease in LC3 protein expression levels (P＜0.05). ConclusionAngelicone may inhibit autophagy in human endometrial cancer RL95-2 cells by regulating the PI3K/Akt/mTOR signaling pathway. |
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