Oxidative Stress in Cancer Biology

Dear Colleagues,

Cellular oxidative stress results from an imbalance between pro-oxidant and antioxidant mechanisms due to either increased production of free oxygen radicals and/or deficiency of antioxidant mechanisms. Under physiological conditions, in a normal cell, there is continuous production of free oxygen radicals. It is well established that free radicals are products of normal cellular metabolism and have a dual role that could be either beneficial or harmful for the cell. Thus, low levels of free oxygen radicals modulate cell signaling, initiate pathways of cellular stress response, and mediate cellular differentiation, gene transcription, cellular proliferation, and apoptosis. In addition, mild oxidative stress enables cellular adaptation to conditions of severe oxidative stress.  On the other hand, high levels of free oxygen radicals are toxic for the cells due to oxidative damage to cellular constituents such as DNA, lipids, proteins, and sugars. The cells have developed antioxidant mechanisms that combat oxidative stress and ensure redox homeostasis, the balance between pro-oxidant and antioxidant substances. Antioxidant mechanisms include antioxidant enzymes and non-enzymatic antioxidants. 

Oxidative stress is implicated in the pathogenesis of a number of diseases, including cancer development. Importantly, oxidative stress is implicated in the initiation, promotion, and progression of cancer as well as in metastasis. The mechanisms underlying the effect of oxidative stress in the cancer process are not fully delineated. This Special Issue invites papers that contribute knowledge to the molecular mechanisms that link oxidative stress with cancer.

Dr. Eugenia Yiannakopoulou
Guest Editor

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