AI Article Synopsis
- The study explores how the hormone 17beta-estradiol (E2) affects oxidative stress and certain proteins in breast cancer cells, focusing on estrogen receptors ERalpha and ERbeta.
- In breast tumors, the ratio of ERalpha to ERbeta is higher compared to normal tissue, which may influence how these cells respond to oxidative stress.
- The research found that cell lines with different ERalpha/ERbeta ratios (like T47D and MCF-7) exhibited distinct responses: T47D had low reactive oxygen species (ROS) and high UCP5, while MCF-7 showed high oxidative stress along with increased antioxidant enzyme levels, but decreased UCP2 and worsening oxidative damage.
Article Abstract
The effects of 17beta-estradiol (E2) are mediated through activation of estrogen receptors (ER): ERalpha and ERbeta. It is known that ERalpha/ERbeta ratio is higher in breast tumors than in normal tissue. Since antioxidant enzymes and uncoupling proteins (UCPs) are reactive oxygen species (ROS) production and mitochondrial biogenesis regulators, our aim was to study the E2-effect on oxidative stress, antioxidant enzyme expression, and UCPs in breast cancer cell lines with different ERalpha/ERbeta ratios. The lower ERalpha/ERbeta ratio T47D cell line showed low ROS production and high UCP5 levels. However, the higher ERalpha/ERbeta ratio MCF-7 cell line showed an up-regulation of antioxidant enzymes and UCPs, yet exhibited high oxidative stress. As a result, a decrease in antioxidant enzyme activities and UCP2 protein levels, coupled with an increase in oxidative damage was found. On the whole, these results show different E2-effects on oxidative stress regulation, modulating UCPs, and antioxidant enzymes, which were ERalpha/ERbeta ratio dependent in breast cancer cell lines.
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| http://dx.doi.org/10.1002/jcb.24192 | DOI Listing |
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