Suppr超能文献

瑞戈非尼通过诱导自噬来延缓肝细胞癌的增殖。

Regorafenib delays the proliferation of hepatocellular carcinoma by inducing autophagy.

作者信息

Han Rui, Li Shixin

出版信息

Pharmazie. 2018 Apr 2;73(4):218-222. doi: 10.1691/ph.2018.7988.

Abstract

The aim of the present study was to investigate the effects of regorafenib on hepatocellular carcinoma autophagy, thereby supressing the malignancy of HCC. First, HepG2 and Hep3B cell autophagy was investigated using GFP-LC3 transfection after the treatment of regorafenib. Then, the activation of Akt/mTOR signaling was analyzed using western blot. Our data showed that liver cancer cell autophagy was significantly induced by 20 μM regorafenib using GFP-LC3 transfection. Meanwhile, regorafenib-induced cell death could largely be abolished by 3-MA or CQ treatment, suggesting that regorafenib-induced HepG2 cell death was partially dependent on autophagy. Moreover, the activation of Akt/mTOR signaling was inhibited by regorafenib pre-incubation. MTT assay showed the combination use of regorafenib and CDDP led to a stronger growth inhibitory effect on HepG2 and Hep3B cells. In summary, regorafenib may acts an adjunctive therapy for liver cancer patients via modulating autophagy-dependent cell death even when apoptosis resistance is induced in cancer cells.

摘要

本研究的目的是探讨瑞戈非尼对肝细胞癌自噬的影响,从而抑制肝癌的恶性程度。首先,在瑞戈非尼处理后,使用绿色荧光蛋白标记的微管相关蛋白轻链3(GFP-LC3)转染来研究HepG2和Hep3B细胞的自噬。然后,使用蛋白质免疫印迹法分析Akt/mTOR信号通路的激活情况。我们的数据显示,使用GFP-LC3转染时,20μM瑞戈非尼可显著诱导肝癌细胞自噬。同时,3-甲基腺嘌呤(3-MA)或氯喹(CQ)处理可在很大程度上消除瑞戈非尼诱导的细胞死亡,这表明瑞戈非尼诱导的HepG2细胞死亡部分依赖于自噬。此外,瑞戈非尼预孵育可抑制Akt/mTOR信号通路的激活。噻唑蓝(MTT)法检测显示,瑞戈非尼与顺铂(CDDP)联合使用对HepG2和Hep3B细胞具有更强的生长抑制作用。总之,即使癌细胞诱导了凋亡抗性,瑞戈非尼仍可能通过调节自噬依赖性细胞死亡,作为肝癌患者的辅助治疗手段。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验