Abstract
Conversely to normal cells, where deregulated oxidative stress drives the activation of death pathways, malignant cells exploit oxidative milieu for its advantage. Cancer cells are located in a very complex microenvironment together with stromal components that participate to enhance oxidative stress to promote tumor progression. Indeed, convincing experimental and clinical evidence underline the key role of oxidative stress in several tumor aspects thus affecting several characteristics of cancer cells. Oxidants influence the DNA mutational potential, intracellular signaling pathways controlling cell proliferation and survival and cell motility and invasiveness as well as control the reactivity of stromal components that is fundamental for cancer development and dissemination, inflammation, tissue repair, and de novo angiogenesis. This paper is focused on the role of oxidant species in the acquisition of two mandatory features for aggressive neoplastic cells, recently defined by Hanahan and Weinberg as new “hallmarks of cancer”: tumor microenvironment and metabolic reprogramming of cancer cells.
Highlights
With over 3 million novel cases each year in Europe, cancer is a main public health hitch with a vital need for new therapies
Human prostate CAFs exert their propelling role for Epithelial Mesenchymal Transition (EMT) in strict dependence on cycloxygenase-2 (COX-2), Nuclear Factor κ-B (NF-κB), and hypoxia-inducible factor (HIF-)1, due to COX-2-mediated release of reactive oxygen species, which is mandatory for EMT, stemness, and dissemination of metastatic cells [48, 59]
The paper of Mateescu et al demonstrates that high-grade human ovarian adenocarcinomas that accumulate miR-200a contain high level of Reactive Oxygen Species (ROS), which correlate with improved survival of patients in response to treatment and conclude that oxidative stress promotes tumor growth, it sensitizes tumor to treatment, which could account for the limited success of antioxidants in clinical trials [84]
Summary
With over 3 million novel cases each year in Europe, cancer is a main public health hitch with a vital need for new therapies. Positively affects mandatory steps of cancer initiation and progression, by acting on cell proliferation and anchorage independent cell growth, causing insensitivity to apoptosis, sustaining de novo angiogenesis, and by altering the migration/invasion programme through metabolic and epigenetic mechanisms (Figure 1). In this scenario, Reactive Oxygen Species (ROS) exert a key role affecting several hallmarks of cancer. Both features, enabling cancer cells to achieve a more aggressive phenotype, have been correlated to oxidative stress and will be described below
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