Effects of Amarogentin on Residual Liver Cancer Stem Cells After Insufficient Thermal Ablation and Related Mechanism
10.3971/j.issn.1000-8578.2023.22.1528
- VernacularTitle:苦龙胆酯苷对热消融不全的残存肝癌干细胞的影响及机制初探
- Author:
Yan LIU
1
;
Fanbo QIN
;
Jianping GONG
;
Wenfeng ZHANG
Author Information
1. Geriatric Diseases Institute of Chengdu/Cancer Prevention and Treatment Institute of Chengdu, Digestive System Department, Chengdu Fifth People's Hospital (the Second Clinical Medical College), Affiliated Fifth People's Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China
- Publication Type:Research Article
- Keywords:
Amarogentin;
Insufficient thermal ablation;
Liver cancer stem cells;
TBC1D15;
p53
- From:
Cancer Research on Prevention and Treatment
2023;50(8):760-766
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of amarogentinon liver cancer stem cells (LCSCs) after insufficient thermal ablation and its mechanism. Methods A insufficient thermal ablation model of HepG2 cells was established by water bath method.The percentage of CD133-positive LCSCs and the mRNA and protein levels of CD133 were detected by flow cytometry, qRT-PCR and Western blot.The insufficient thermal ablation model of HepG2 cells was treated with variable doses of amarogentin for 24 h; the percentage of CD133-positive LCSCs, the proliferation and apoptosis of liver cancer cells, and the mRNA and protein levels of CD133, TBC1D15, and p53were detected by flow cytometry, qRT-PCR and Western blot. Results The percentage of CD133-positive HepG2 cells and the mRNA and protein levels of CD133 and TBC1D15in the insufficient thermal ablation model were significantly higher than those in the normal HepG2 cells.Amarogentin then markedly decreased the percentage of CD133-positive LCSCs, the proliferation rate of HepG2 cells, and the mRNA and protein levels of CD133 and TBC1D15 in the insufficient thermal ablationresidual model (all P < 0.05);inversely, the apoptosis rate of HepG2 cells and the phosphorylated levels of p53 in the insufficient thermal ablation model were significantly increased (all P < 0.05). Conclusion Amarogentin could reduce the proportion of LCSCs after insufficient thermal ablation, inhibit the proliferation, and promote the apoptosis of LCSCs, which maybe associated with increasing the phosphorylation of p53 and inhibiting the expression of TBC1D15.
