Cancer drug resistance: redox resetting renders a way
Metrics: PDF 1867 views | HTML 3309 views | ?
Yuan Liu1,2,*, Qifu Li2,*, Li Zhou1,*, Na Xie1, Edouard C. Nice3, Haiyuan Zhang2, Canhua Huang1 and Yunlong Lei4
1 State Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, P. R. China
2 Department of Neurology, The Affiliated Hospital of Hainan Medical College, Haikou, Hainan, P. R. China
3 Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia
4 Department of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, P. R. China
* These authors have contributed equally to this work
Yunlong Lei, email:
Canhua Huang, email:
Haiyuan Zhang, email:
Keywords: drug resistance, cancer therapy, oxidative stress, redox modifications, drug efflux
Received: October 28, 2015 Accepted: March 28, 2016 Published: April 05, 2016
Disruption of redox homeostasis is a crucial factor in the development of drug resistance, which is a major problem facing current cancer treatment. Compared with normal cells, tumor cells generally exhibit higher levels of reactive oxygen species (ROS), which can promote tumor progression and development. Upon drug treatment, some tumor cells can undergo a process of ‘Redox Resetting’ to acquire a new redox balance with higher levels of ROS accumulation and stronger antioxidant systems. Evidence has accumulated showing that the ‘Redox Resetting’ enables cancer cells to become resistant to anticancer drugs by multiple mechanisms, including increased rates of drug efflux, altered drug metabolism and drug targets, activated prosurvival pathways and inefficient induction of cell death. In this article, we provide insight into the role of ‘Redox Resetting’ on the emergence of drug resistance that may contribute to pharmacological modulation of resistance.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.