期刊
ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY
卷 48, 期 1, 页码 488-497出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/21691401.2019.1709862
关键词
Hepatocellular carcinoma (HCC); apoptosis; cell cycle arrest; reactive oxygen species (ROS); autophagy; p53; DRAM; ER stress
资金
- Sanming Project of Medicine in Shenzhen [SZSM201612021]
- Special Foundation for Science and Technology Development of Guangdong Province [2017B090904010]
- Scientific Research Project of Health and Family Planning Commission of Shenzhen Municipality [SZXJ2018086]
Human hepatocellular carcinoma (HCC) is the most common type of liver cancer, and it has a high mortality rate. Despite surgical treatments, radiotherapy, and chemotherapy, the median survival of patients with advanced HCC is low. Evidence has shown that tanshinone (TA) I exhibits anti-proliferative activity against numerous cancers. However, the role of TA I and its mechanism in HCC remain unknown. Here, we determined the anti-cancer potential of TA I against HCC cell lines HepG2 and Huh7. Cell viability was analyzed using a Cell Counting Kit-8 assay. Flow cytometry was used to analyze cell cycles and apoptosis. Western blotting was used to detect protein expression and phosphorylation levels. TA I was found to inhibit cell proliferation, induce G0/G1 phase arrest, and trigger apoptosis in HepG2 and Huh7 cells. We further explored the molecular mechanism of TA I-mediated apoptosis. Our results showed that TA I induced G0/G1 phase arrest through downregulation of cyclin D1 expression and upregulation of p21 expression. TA I induced cell apoptosis via reactive oxygen species-mediated endoplasmic reticulum stress and by inhibiting p53/damage-regulated autophagy modulator (DRAM)-mediated autophagy in HepG2 and Huh7 cells. Therefore, TA I may be an anti-cancer drug candidate in the treatment of HCC.
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