Dioscin inhibits human endometrial carcinoma proliferation via G0/G1 cell cycle arrest and mitochondrial-dependent signaling pathway. (February 2021)

• Record Type: Journal Article
• Authors: Li, Xiao-Li; Ma, Run-Hui; Ni, Zhi-Jing; Thakur, Kiran; Cespedes-Acuña, Carlos L.; Wang, Shaoyun; Zhang, Jian-Guo; Wei, Zhao-Jun
• Is Part Of: Food and chemical toxicology. Volume 148(2021)
• Publication Date: 2021-02
• Subjects: Dioscin -- Ishikawa -- Cell cycle -- Apoptosis -- Mitochondrial pathway; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2020.111941
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: The present study emphasized on the anti-cancerous effects of dioscin and its underlying molecular mechanism in human endometrial cancer Ishikawa cells. Dioscin significantly suppressed the proliferation of Ishikawa cells at IC50 of 2.37 μM. Besides, dioscin could inhibit the proliferation of Ishikawa cells by blocking the G0/G1 cell cycle through up-regulation of p16, p21, and p27 and down-regulation of cycle-cellular protein (Cyclin A/D/E) and cyclin-dependent kinase (CDK2/4/6). Also, it promoted apoptosis through the mitochondrial pathway, including the regulation of Bcl family proteins, the increase of ROS levels, the activation of caspases (Caspase 9/3), and the decrease of mitochondrial membrane permeability. Whereas dioscin also effectively activated the marker genes and proteins (Fas, TNF-R1, and Caspase 8) related to the death receptor-mediated pathway which confirmed the involvement of both the pathways for dioscin-induced apoptosis. The current results demonstrated that dioscin possessed potential health benefits with respect to endometrial cancer prevention and treatment. Graphical abstract: Image 1 Highlights: Dioscin inhibited Human Endometrial Carcinoma proliferation in Ishikawa cells. Dioscin arrested Ishikawa cells at G1/G0 phase through the regulation of cycle-related signals. Dioscin induced apoptosis by activating the mitochondrial and the death receptor pathways.