Calycosin induces mitochondrial-dependent apoptosis and cell cycle arrest, and inhibits cell migration through a ROS-mediated signaling pathway in HepG2 hepatocellular carcinoma cells. (February 2021)

• Record Type: Journal Article
• Authors: Liu, Yang; Piao, Xian-Ji; Xu, Wan-Ting; Zhang, Yu; Zhang, Tong; Xue, Hui; Li, Yan-Nan; Zuo, Wen-Bo; Sun, Geng; Fu, Zhong-Ren; Luo, Ying-Hua; Jin, Cheng-Hao
• Is Part Of: Toxicology in vitro. Volume 70(2021)
• Publication Date: 2021-02
• Subjects: Calycosin -- Hepatocellular carcinoma -- Apoptosis -- Cell cycle arrest -- Reactive oxygen species -- Cell migration; Toxicity testing -- In vitro -- Periodicals; Toxicology -- Periodicals; 615.9
• DOI: 10.1016/j.tiv.2020.105052
• Languages: English
• ISSNs: 0887-2333

Abstract

Abstract: Calycosin is one of the main ingredients extracted from the Chinese medical herb, Radix astragali (RA). It has been shown to inhibit cell proliferation and induce apoptosis in several cancer cell lines, but the underlying mechanism remains unclear. The effects of calycosin on the proliferation and apoptosis of hepatocellular carcinoma (HCC) cells, as well as its mechanism, were investigated in this study. Cell Counting Kit-8 assay results suggested that calycosin had anti-proliferation effects on HCC in dose- and time-dependent manners, and had less cytotoxicity in normal cells. Hoechst/PI double staining and flow cytometry results showed cellular morphological changes and apoptosis after treatment of HepG2 cells with calycosin. The western blot assay showed calycosin decreased the expression of Bcl-2 and increased the expression of Bax, caspase-3, and PARP. Calycosin induced the activation of MAPK, STAT3, NF-κB, apoptosis-related proteins, and induced cell cycle arrest in the G0/G1 phase by regulating AKT. In addition, calycosin reduced the expression of TGF-β1, SMAD2/3, SLUG, and vimentin. Furthermore, phosphorylation, apoptosis, and cell migration induced by calycosin were mediated by the production of reactive oxygen species. These events could be inhibited by pretreatment with N -acetyl-L-cysteine. Calycosin resisted HCC by activating ROS-mediated MAPK, STAT3, and NF-κB signaling pathways. Highlights: Calycosin induces apoptosis by activating MAPK, STAT3, and NF-κB signaling pathways. Calycosin induces cell cycle arrest in G0/G1 phase via AKT signaling pathways. Calycosin inhibits cell migration by TGF-β1 signaling pathways.