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.
Highlights
Reactive oxygen species (ROS), as second messengers, function in various cellular signal pathways in normal cells and cancer cells [1]
Most of drug or growth factors induce downstream cascades that result in short-lived reactive oxygen species (ROS) generation
Cancer cells regulate the redox homeostasis to survival
Summary
Reactive oxygen species (ROS), as second messengers, function in various cellular signal pathways in normal cells and cancer cells [1]. [3,10] This process is regulated locally by ROS inducers and antioxidant modules to overcome the possibility that the alternative ROS can affect whole cells [3]. Cancer cells show enhanced glycolysis-mediated metabolisms to overcome over-utilized ATP or alter cellular signal pathways [11]. Chemotherapeutic agents can induce increased ROS levels, and most cancer cells treated with chemotherapy suffer from ROS-mediated apoptosis [12]. Alternative levels of ROS induce DNA damage or transcription factors (TFs)-mediated produced intracellularly is gene expression the superoxide nucleus. ROS regulate cellular processes such as by catalase and peroxiredoxin (Prx).
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