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Cancer Chemotherapy and Chemiluminescence Detection of Reactive Oxygen Species in Human Semen
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Redox-Mediated Mechanism of Chemoresistance in Cancer Cells

Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Korea
Department of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Korea
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(10), 471;
Received: 18 September 2019 / Revised: 7 October 2019 / Accepted: 8 October 2019 / Published: 10 October 2019
(This article belongs to the Special Issue Free Radical Research in Cancer)
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. View Full-Text
Keywords: reactive oxygen species; antioxidant proteins; chemoresistance; oxaliplatin; 5-Fluorouracil reactive oxygen species; antioxidant proteins; chemoresistance; oxaliplatin; 5-Fluorouracil
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Kim, E.-K.; Jang, M.; Song, M.-J.; Kim, D.; Kim, Y.; Jang, H.H. Redox-Mediated Mechanism of Chemoresistance in Cancer Cells. Antioxidants 2019, 8, 471.

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