作者: Xīn Gào , Ben Schöttker
DOI: 10.18632/ONCOTARGET.17128
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摘要: // Xīn Gao 1,2 and Ben Schottker 1,2,3 1 Division of Clinical Epidemiology Aging Research, German Cancer Research Center, Heidelberg, Germany 2 Network University 3 Institute Health Care Social Sciences, FOM University, Essen, Correspondence to: Schottker, email: Keywords : neoplasm; oxidative stress; redox signaling; signal transduction; reactive oxygen species Received November 04, 2016 Accepted April 03, 2017 Published 16, Abstract Oxidative stress results from an imbalance the species/reactive nitrogen (ROS/RNS) production oxidants defense system. Extensive research during last decades has revealed that can mediate cancer initiation development by leading not only to molecular damage but also a disruption reduction–oxidation (redox) signaling. In order provide global overview signaling pathways, which play role in formation, we conducted systematic literature search PubMed ISI Web Science identified 185 relevant reviews published 10 years. The 20 most frequently described pathways were selected be presented this review could categorized into groups: Intracellular ROS/RNS generating organelles enzymes, transduction cascades kinases/phosphatases transcription factors. generation are mitochondria, endoplasmic reticulum peroxisomes. Enzymes, including NOX, COX, LOX NOS, prominent enzymes ROS/RNS. act as messengers transmembrane receptors trigger activation or inhibition kinases/phosphatases, such family members protein tyrosine kinases phosphatases. Furthermore, these reactions activate downstream kinase MAPK cascade, PI3K PKC. phosphatases regulate phosphorylation status factors APE1/Ref-1, HIF-1α, AP-1, Nrf2, NF-κB, p53, FOXO, STAT, β-catenin. Finally, briefly discuss prevention treatment opportunities, address further needs.