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- Title
Redox-Mediated Mechanism of Chemoresistance in Cancer Cells.
- Authors
Kim, Eun-Kyung; Jang, MinGyeong; Song, Min-Jeong; Kim, Dongwoo; Kim, Yosup; Jang, Ho Hee
- Abstract
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.
- Subjects
CANCER cells; NICOTINAMIDE adenine dinucleotide phosphate; CELL cycle; DRUG tolerance; ADENOSINE triphosphate; ENDOPLASMIC reticulum
- Publication
Antioxidants, 2019, Vol 8, Issue 10, p471
- ISSN
2076-3921
- Publication type
Article
- DOI
10.3390/antiox8100471