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Redox regulation in cancer: a double-edged sword with therapeutic potential Acharya A; Das I; Chandhok D; Saha TOxid Med Cell Longev 2010[Jan]; 3 (1): 23-34Oxidative stress, implicated in the etiology of cancer, results from an imbalance in the production of reactive oxygen species (ROS) and cell's own antioxidant defenses. ROS deregulate the redox homeostasis and promote tumor formation by initiating an aberrant induction of signaling networks that cause tumorigenesis. Ultraviolet (UV) exposures, gamma-radiation and other environmental carcinogens generate ROS in the cells, which can exert apoptosis in the tumors, thereby killing the malignant cells or induce the progression of the cancer growth by blocking cellular defense system. Cancer stem cells take the advantage of the aberrant redox system and spontaneously proliferate. Oxidative stress and gene-environment interactions play a significant role in the development of breast, prostate, pancreatic and colon cancer. Prolonged lifetime exposure to estrogen is associated with several kinds of DNA damage. Oxidative stress and estrogen receptor-associated proliferative changes are suggested to play important roles in estrogen-induced breast carcinogenesis. BRCA1, a tumor suppressor against hormone responsive cancers such as breast and prostate cancer, plays a significant role in inhibiting ROS and estrogen mediated DNA damage; thereby regulate the redox homeostasis of the cells. Several transcription factors and tumor suppressors are involved during stress response such as Nrf2, NF-kappaB and BRCA1. A promising strategy for targeting redox status of the cells is to use readily available natural substances from vegetables, fruits, herbs and spices. Many of the phytochemicals have already been identified to have chemopreventive potential, capable of intervening in carcinogenesis.|Animals[MESH]|Antineoplastic Agents, Phytogenic/therapeutic use[MESH]|Antioxidants/metabolism[MESH]|Humans[MESH]|Neoplasms/drug therapy/*metabolism/prevention & control[MESH]|Neoplastic Stem Cells/metabolism[MESH]|Oxidation-Reduction/drug effects[MESH]|Oxidative Stress/drug effects/physiology[MESH]|Reactive Oxygen Species/metabolism[MESH] |
