期刊
ANTIOXIDANTS
卷 8, 期 10, 页码 -出版社
MDPI
DOI: 10.3390/antiox8100471
关键词
reactive oxygen species; antioxidant proteins; chemoresistance; oxaliplatin; 5-Fluorouracil
资金
- National Research Foundation of Korea (NRF) - Korea government [NRF-2017R1D1A1B03035550]
- National Research Foundation of Korea (NRF)
- Center for Women In Science, Engineering and Technology (WISET) - Ministry of Science, ICT & Future Planning of Korea (MSIP) under the Program for Returners into RD
Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer.
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