Reactive oxygen species: A double-edged sword in oncogenesis

Abstract

Reactive oxygen species (ROS) are molecules or ions formed by the incomplete one-electron reduction of oxygen. Of interest, it seems that ROS manifest dual roles, cancer promoting or cancer suppressing, in tumorigenesis. ROS participate simultaneously in two signaling pathways that have inverse functions in tumorigenesis, Ras-Raf-MEK1/2-ERK1/2 signaling and the p38 mitogen-activated protein kinases (MAPK) pathway. It is well known that Ras-Raf-MEK1/2-ERK1/2 signaling is related to oncogenesis, while the p38 MAPK pathway contributes to cancer suppression, which involves oncogene-induced senescence, inflammationinduced cellular senescence, replicative senescence, contact inhibition and DNA-damage responses. Thus, ROS may not be an absolute carcinogenic factor or cancer suppressor. The purpose of the present review is to discuss the dual roles of ROS in the pathogenesis of cancer, and the signaling pathway mediating their role in tumorigenesis.

NF-κB and STAT3 signaling pathways collaboratively link inflammation to cancer

“…During tumor initiation, an infl ammatory microenvironment can enhance the proliferation of mutated cells (Hussain and Harris, 2007;Polyak et al, 2009;Wang et al, 2010). In addition, inflammatory cells can also increase mutation rates through serving as sources of reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI) that are able to induce DNA damage and genomic instability (Miletic et al, 2007;Faux et al, 2009;Pan et al, 2009;Hursting and Berger, 2010;Zargan et al, 2011). The process of tumor growth from a single initiating cell into a fully developed primary tumor is called tumor promotion, which is stimulated by infl ammation-driven mechanism.…”

Reduced NADPH oxidase type 2 activity mediates sleep fragmentation-induced effects on TC1 tumors in mice

“…3 These observations led us to further explore the nature of the molecular mechanisms underlying the pro-cancerigenic activities of SF. Given the critical role of ROS in the pathogenesis of most cancers, [18][19] we hypothesized that Nox2-mediated oxidative stress contributes to SF-induced tumor growth and progression. To test this hypothesis, we used a gp91 phox-/Y mouse model, which lacks the catalytic core subunit (gp91) of the Nox2 enzyme complex and is therefore deficient in Nox2 activity.…”

Effect of ELF-EMF on antioxidant status and micronuclei in K562 cells and normal lymphocytes

“…It is well known that Ras-Raf-MEK1/2-ERK1/2 signaling is related to oncogenesis, while the p38 MAPK pathway contributes to cancer suppression. Thus, ROS may not be an absolute carcinogenic factor or cancer suppressor [15].…”