首页> 外文OA文献 >Myricetin induces apoptosis and autophagy by inhibiting PI3K/Akt/mTOR signalling in human colon cancer cells
【2h】

Myricetin induces apoptosis and autophagy by inhibiting PI3K/Akt/mTOR signalling in human colon cancer cells

机译:Myricetin通过抑制人结肠癌细胞中的pi3k / akt / mtor信号传导来诱导细胞凋亡和自噬

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Abstract Background The compound 3,3′,4′,5,5′,7-hexahydroxyflavone (myricetin) is a natural flavonoid with antitumour activity. Most of the studies on myricetin have focused on the induction of tumour cell apoptosis, and little is known about the regulatory effects of myricetin on autophagy in colorectal cancer. Methods Here, we studied the effects of myricetin on colon cancer cell proliferation, apoptosis and autophagy. We detected colon cancer cell apoptosis induced by myricetin via flow cytometry and Hoechst 33258 staining. Transmission electron microscopy was performed to observe the morphological changes associated with autophagy. The expression levels of apoptosis-, autophagy- and PI3K/Akt/mTOR signalling-related proteins were measured by Western blot analysis. Results This study confirmed that myricetin inhibits the proliferation of 4 kinds of colon cancer cell lines. Myricetin induced cell apoptosis and autophagy by inhibiting PI3K/Akt/mTOR signalling pathway. In addition, the inhibition of autophagy with 3-methyladenine (3-MA) promoted the apoptosis of myricetin-treated colon cancer cells. Conclusions Considering that myricetin induces apoptosis and autophagy in colon cancer cells, myricetin may become a viable candidate for chemotherapy; it could be used to exert tumour inhibitory effects alone or as adjuvant chemotherapy to inhibit autophagy. These studies may provide further evidence for the potential use of myricetin in the treatment of colon cancer.
机译:摘要背景化合物3,3',4',5,5',7-六羟基吡喃酮(Myricetin)是一种天然黄酮,具有抗肿瘤活性。大多数关于Myricetin的研究都集中在肿瘤细胞凋亡的诱导上,并且关于Myricetin对结直肠癌自噬的调节作用很少。方法在这里,我们研究了Myricetin对结肠癌细胞增殖,细胞凋亡和自噬的影响。我们通过流式细胞术和Hoechst 33258染色检测了Myricetin诱导的结肠癌细胞凋亡。进行透射电子显微镜检查以观察与自噬相关的形态变化。通过蛋白质印迹分析测量凋亡,自噬和PI3K / AKT / MTOR信号传导相关蛋白的表达水平。结果本研究证实,Myricetin抑制4种结肠癌细胞系的增殖。通过抑制PI3K / AKT / MTOR信号传导途径诱导细胞凋亡和自噬。此外,用3-甲基腺嘌呤(3-mA)的自噬抑制促进了Myricetin治疗的结肠癌细胞的凋亡。结论考虑到霉菌素诱导结肠癌细胞中凋亡和自噬,Myricetin可能成为化疗的可行候选者;它可用于单独施用肿瘤抑制作用或作为辅助化学疗法以抑制自噬。这些研究可以提供进一步证据潜在使用Myricetin治疗结肠癌。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号