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叶文蔚,潘丹,杨晶金,吴静怡,蔡仙丽.苦杏仁苷调控PI3K/Akt/mTOR通路对子宫内膜癌细胞增殖、侵袭及凋亡的影响[J].浙江中西医结合杂志,2020,30(10):
苦杏仁苷调控PI3K/Akt/mTOR通路对子宫内膜癌细胞增殖、侵袭及凋亡的影响
Effects of amygdalin on proliferation, invasion and apoptosis of endometrial cancer cells through inhibiting the PI3K / Akt / mTOR pathway
投稿时间:2020-05-07  修订日期:2020-08-18
DOI:
中文关键词:  苦杏仁苷  子宫内膜癌  细胞增殖  细胞侵袭;细胞凋亡  PI3K/Akt/mTOR通路
英文关键词:amygdalin  Endometrial cancer  Cell proliferation  Cell invasion  Apoptosis  PI3K/Akt/mTOR signaling pathway
基金项目:浙江省医药卫生科技计划项目(No.2019RC312),台州学院培育项目(No.2018PY69)
作者单位E-mail
叶文蔚 台州市立医院 ywwfuke@163.com 
潘丹 台州市立医院  
杨晶金 台州市立医院  
吴静怡 台州市立医院  
蔡仙丽 台州市立医院 cxlfuke@163.com 
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中文摘要:
      目的 研究苦杏仁苷对子宫内膜癌RL95-2、HEC-1B细胞增殖、侵袭及凋亡的影响,并探讨PI3K/Akt/mTOR信号通路在其中发挥的作用。方法 使用不同浓度(8 mg/L、16 mg/L、32 mg/L、64 mg/L、128 mg/L)苦杏仁苷处理子宫内膜癌RL95-2、HEC-1B细胞不同时间(24 h、48 h、72 h)后,采用CCK-8法检测各组细胞的增殖能力并计算苦杏仁苷的半数抑制浓度(IC50);Transwell试验检测苦杏仁苷对细胞的侵袭能力的影响;流式细胞仪检测各组细胞凋亡情况;Western Blot实验检测凋亡相关基因Bcl-2、Bax蛋白以及PI3K/Akt/mTOR信号通路相关蛋白的表达情况。结果 苦杏仁苷呈浓度及时间依赖性抑制子宫内膜癌RL95-2、HEC-1B细胞的生长活性,苦杏仁苷在48 h时的半数抑制浓度(IC 50)约为40 mg/L;苦杏仁苷能抑制子宫内膜癌细胞穿膜细胞数[RL95-2:(227±11.06)比(459±24.75),P<0.01; HEC-1B:(188±11.14)比(412±14),P<0.01];经苦杏仁苷处理后细胞凋亡率升高[RL95-2:(7.85%±0.71%)比(1.49%±0.08%),P<0.01; HEC-1B:(8.55%±0.69%)比(1.61%±0.13%),P<0.01],凋亡蛋白Bcl-2表达下降[RL95-2:(0.45±0.03)比(1.02±0.08),P<0.01; HEC-1B:(0.56±0.07)比(1.03±0.06),P<0.01],Bax表达升高[RL95-2:(2.04±0.05)比(1.05±0.05),P<0.01; HEC-1B:(2.44±0.10)比(1.01±0.04),P<0.01];此外,苦杏仁苷能显著下调PI3K [RL95-2:(0.42±0.04)比(1.01±0.05),P<0.01; HEC-1B:(0.36±0.05)比(1.02±0.03),P<0.01]、AKT [RL95-2:(0.73±0.05)比(1.02±0.05),P<0.01; HEC-1B:(0.65±0.03)比(1.03±0.04),P<0.01]及mTOR [RL95-2:(0.25±0.04)比(1.03±0.06),P<0.01; HEC-1B:(0.34±0.05)比(1.05±0.04),P<0.01]的磷酸化水平,抑制PI3K/Akt/mTOR通路活化。结论 苦杏仁苷通过抑制PI3K/Akt/mTOR信号通路活化,促进子宫内膜癌RL95-2、HEC-1B细胞凋亡,降低其增殖活性,抑制细胞侵袭功能,从而发挥抗肿瘤作用。
英文摘要:
      Objective To study the effect of amygdalin on the proliferation, invasion and apoptosis of endometrial cancer RL95-2、HEC-1B cells, and to explore the role of the PI3K/Akt/mTOR signaling pathway. Method Different concentrations (8 mg/L, 16 mg/L, 32 mg/L, 64 mg/L, 128 mg/L) of amygdalin treated endometrial cancer RL95-2、HEC-1B cells for different times (24 h, 48 h, 72 h), CCK-8 method was used to detect the proliferation of cells in each group and calculate the half inhibitory concentration of amygdalin (IC50); Transwell test was used to detect the effect of amygdalin on cell migration; Flow cytometry was applied to detect apoptosis in each group; The expression of Bcl-2, Bax and PI3K/Akt/mTOR signaling pathway related proteins were detected by Western blot. Result Amygdalin inhibited the growth of endometrial cancer cells in a dose- and time-dependent manner, the IC50 of amygdalin at 48 h was about 40 mg/L; In addition, amygdalin significantly decreased the number of transmembrane cells[RL95-2:(227±11.06)vs(459±24.75),P<0.01; HEC-1B:(188±11.14)vs(412±14),P<0.01]; Apoptosis rate was increased by amygdalin[RL95-2:(7.85%±0.71%)vs(1.49%±0.08%),P<0.01; HEC-1B:(8.55%±0.69%)vs(1.61%±0.13%),P<0.01],meanwhile, the expression of the anti-apoptoses gene Bcl-2 was downregulated by amygdalin[RL95-2:(0.45±0.03)vs(1.02±0.08),P<0.01; HEC-1B:(0.56±0.07)vs(1.03±0.06),P<0.01], and the expression of pro-apoptosis gene Bax was upregulated at the protein levels[RL95-2:(2.04±0.05)vs(1.05±0.05),P<0.01; HEC-1B:(2.44±0.10)vs(1.01±0.04),P<0.01]. In addition, amygdalin can inhibit the PI3K/Ak/mTOR pathway and significantly downregulate the protein levels of p-PI3K [RL95-2:(0.42±0.04)vs(1.01±0.05),P<0.01; HEC-1B:(0.36±0.05)vs(1.02±0.03),P<0.01]、p-Akt [RL95-2:(0.73±0.05) vs (1.02±0.05),P<0.01; HEC-1B:(0.65±0.03) vs(1.03±0.04),P<0.01] and p-mTOR [RL95-2:(0.25±0.04)vs (1.03±0.06),P<0.01; HEC-1B:(0.34±0.05)vs(1.05±0.04),P<0.01]. Conclusion Amygdalin inhibits the activation of PI3K/Akt/mTOR signaling pathway, promotes endometrial cancer cell apoptosis, reduces its proliferative activity, inhibits cell invasion, and thus exerts antitumor effects.
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