周術期医学ジャーナル
オープンアクセス
ISSN: 2576-1471
ISSN: 2576-1471
Elie Hatem* and Sandy Azzi*
Oxidative stress results from a disequilibrium between production and their elimination by cellular antioxidant systems. This leads to the accumulation of ROS that have a deleterious effect on vital biological macromolecules. It is now well established that cancer cells exhibit a pro-oxidant state due to metabolic and genetic abnormalities. The disequilibrium in redox homeostasis in cancer cells promotes genomic instability leading to the activation of oncogenes, mitochondrial dysfunction and an alteration in antioxidants activities. All these events can further escalate ROS levels, causing more DNA damage and genetic instability. This vicious cycle is “beneficial” for the process of carcinogenesis and numerous reports have indeed proven the pivotal role of ROS in cancer initiation, cell migration, invasion and metastasis. In order to cope with this sustained redox deregulation, cancer cells, very likely, utilize the full antioxidant capacity of their enzymatic and non-enzymatic systems. Cancer cells are thus highly dependent on their antioxidant systems and especially antioxidant enzymes. Keeping with this, targeting the enzymatic antioxidant system could be an efficient strategy to preferentially kill cancer cells by increasing intracellular ROS levels beyond a certain “threshold” of tolerance eventually leading to specific cancer cell death. In this review we present an overview on ROS generation and focus on the implication of ROS in cancer initiation, epithelial–mesenchymal transition, cell migration, invasion and metastasis, as well as the cancer stem-like phenotype. We finally present different therapeutic approaches that target the enzymatic antioxidant system in order to selectively kill cancer cells.