Abstract
ROS have vital roles in cellular signaling and homeostasis. At low concentration, ROS promotes cancer cell survival by the activation of growth factors and MAP-kinases (MAPKs) that further activates cell cycle progression. At high concentration, ROS produces oxidative stress that activates programmed cell death or apoptosis. However, this fine distinction of ROS action either as a growth promoter or pro-apoptotic agent depends not only on dosage (concentration) but also on the duration, type, and site of ROS generation. The female steroid estrogens and their various metabolites generate ROS in the breast cancer cells. Slow, sustained and moderate level of ROS generated by estrogens and their metabolites cause initiation and progression of breast cancer. ROS generated by estrogens affect pro-proliferative (e.g. cyclin D1, Cdc2), prosurvival (e.g. AKT), antiapoptotic (e.g. BCl2) and pro-inflammatory (e.g. NF-κB) molecules. These multipronged actions of ROS lead to the activation of several signaling pathways involved in the breast cancer cell survival and proliferation, resulting in the progression of breast cancer. Present review article provides insights into the role of estrogen generated ROS and its associated signaling pathways in the initiation and progression of breast cancer. The importance of ROS as breast cancer drug target has also been discussed.
Keywords: Antioxidants, breast cancer, estrogens, prooxidants, reactive oxygen species (ROS), signaling.
Anti-Cancer Agents in Medicinal Chemistry
Title:Role of Reactive Oxygen Species in Estrogen Dependant Breast Cancer Complication
Volume: 16 Issue: 2
Author(s): Ramesh Johar, Rohit Sharma, Amanpreet Kaur and Tapan K. Mukherjee
Affiliation:
Keywords: Antioxidants, breast cancer, estrogens, prooxidants, reactive oxygen species (ROS), signaling.
Abstract: ROS have vital roles in cellular signaling and homeostasis. At low concentration, ROS promotes cancer cell survival by the activation of growth factors and MAP-kinases (MAPKs) that further activates cell cycle progression. At high concentration, ROS produces oxidative stress that activates programmed cell death or apoptosis. However, this fine distinction of ROS action either as a growth promoter or pro-apoptotic agent depends not only on dosage (concentration) but also on the duration, type, and site of ROS generation. The female steroid estrogens and their various metabolites generate ROS in the breast cancer cells. Slow, sustained and moderate level of ROS generated by estrogens and their metabolites cause initiation and progression of breast cancer. ROS generated by estrogens affect pro-proliferative (e.g. cyclin D1, Cdc2), prosurvival (e.g. AKT), antiapoptotic (e.g. BCl2) and pro-inflammatory (e.g. NF-κB) molecules. These multipronged actions of ROS lead to the activation of several signaling pathways involved in the breast cancer cell survival and proliferation, resulting in the progression of breast cancer. Present review article provides insights into the role of estrogen generated ROS and its associated signaling pathways in the initiation and progression of breast cancer. The importance of ROS as breast cancer drug target has also been discussed.
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Cite this article as:
Johar Ramesh, Sharma Rohit, Kaur Amanpreet and Mukherjee K. Tapan, Role of Reactive Oxygen Species in Estrogen Dependant Breast Cancer Complication, Anti-Cancer Agents in Medicinal Chemistry 2016; 16 (2) . https://dx.doi.org/10.2174/1871520615666150518092315
DOI https://dx.doi.org/10.2174/1871520615666150518092315 |
Print ISSN 1871-5206 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5992 |
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