Abstract Title:

Emodin Induces Apoptosis of Colon Cancer Cells via Induction of Autophagy in a ROS-Dependent Manner.

Abstract Source:

Oncol Res. 2017 Jul 25. Epub 2017 Jul 25. PMID: 28762328

Abstract Author(s):

Yuanyuan Wang, Qin Luo, Xianlu He, He Wei, Ting Wang, Jichun Shao, Xinni Jiang

Article Affiliation:

Yuanyuan Wang


Recent studies revealed that emodin extracted from Chinese herbs exhibits an anti-cancer effect on different cancer types, including colon cancer. However, the mechanism is not well understood by now. In our study, we confirmed that emodin treatment inhibited cell viability and induced apoptosis in colon cancer cells. Further experiments were taken to found that emodin was also able to induce autophagy, which is indispensible for apoptosis induced by it. More interestingly, emodin treatment also results in mitochondrial dysfunction and ROS accumulation in those colon cancer cells. Finally, we stressed that ROS accumulation is essential for autophagy and apoptosis induced by emodin. In conclusion, emodin induces apoptosis in clone cancer cells through induction of autophagy, during which ROS generation is of the essence. Our findings improve understanding of emodin's effect on colon cancer suppression and provide new theoretical basis for colon cancer therapy.

Study Type : In Vitro Study

Print Options

Key Research Topics

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2021 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.