4-羟基德里菌素通过调节肝癌细胞中的PI3K/AKT/mTOR信号通路促进细胞凋亡和细胞周期阻滞。

4-Hydroxyderricin Promotes Apoptosis and Cell Cycle Arrest through Regulating PI3K/AKT/mTOR Pathway in Hepatocellular Cells.

作者信息

Gao Xiang, Jiang Yuhuan, Xu Qi, Liu Feng, Pang Xuening, Wang Mingji, Li Qun, Li Zichao

机构信息

Institute of Biomedical Engineering, College of Life Sciences, Qingdao University, Qingdao 266071, China.

Department of Horticultural Technology, Ningbo City College of Vocational Technology, Ningbo 315199, China.

出版信息

Foods. 2021 Aug 29;10(9):2036. doi: 10.3390/foods10092036.

4-hydroxyderricin (4-HD), as a natural flavonoid compound derived from , has largely unknown inhibition and mechanisms on liver cancer. Herein, we investigated the inhibitory effects of 4-HD on hepatocellular carcinoma (HCC) cells and clarified the potential mechanisms by exploring apoptosis and cell cycle arrest mediated via the PI3K/AKT/mTOR signaling pathway. Our results show that 4-HD treatment dramatically decreased the survival rate and activities of HepG2 and Huh7 cells. The protein expressions of apoptosis-related genes significantly increased, while those related to the cell cycle were decreased by 4-HD. 4-HD also down-regulated PI3K, p-PI3K, p-AKT, and p-mTOR protein expression. Moreover, PI3K inhibitor (LY294002) enhanced the promoting effect of 4-HD on apoptosis and cell cycle arrest in HCC cells. Consequently, we demonstrate that 4-HD can suppress the proliferation of HCC cells by promoting the PI3K/AKT/mTOR signaling pathway mediated apoptosis and cell cycle arrest.

4-羟基德里辛（4-HD）作为一种源自[具体来源未给出]的天然黄酮类化合物，其对肝癌的抑制作用及机制在很大程度上尚不清楚。在此，我们研究了4-HD对肝癌细胞（HCC）的抑制作用，并通过探索经由PI3K/AKT/mTOR信号通路介导的细胞凋亡和细胞周期阻滞来阐明其潜在机制。我们的结果表明，4-HD处理显著降低了HepG2和Huh7细胞的存活率和活性。凋亡相关基因的蛋白表达显著增加，而细胞周期相关基因的蛋白表达则被4-HD降低。4-HD还下调了PI3K、p-PI3K、p-AKT和p-mTOR蛋白表达。此外，PI3K抑制剂（LY294002）增强了4-HD对HCC细胞凋亡和细胞周期阻滞的促进作用。因此，我们证明4-HD可通过促进PI3K/AKT/mTOR信号通路介导的细胞凋亡和细胞周期阻滞来抑制HCC细胞的增殖。