Breast cancer is one of the leading causes of mortality among women worldwide due to aggressive behavior, early
metastasis, resistance to existing chemotherapeutic agent and high mortality rate.
Doxorubicin (Dox) is a powerful antitumoral drug. It is one of the most active agents for treatment of
breast cancer. The aim of the present study was to evaluate the influence of Dox in apoptosis and oxidative stress in the
breast cancer cell lines MCF-10F, MCF-7 and MDA-MB-231. These studies showed that Dox decreased anti-apoptotic Bcl-2
protein expression and affected oxidative stress by increasing
hydrogen peroxide production and simultaneously decreasing NF-κB gene and
protein expression in MCF-7, a tumorigenic triple-positive cell line. Results also indicated that Dox induced apoptosis by upregulating Bax,
caspase-8 and
caspase-3 and downregulation of Bcl-2
protein expression. On the contrary, ROS damage decreased by increasing SOD2 gene and
protein expression and
hydrogen peroxide production with parallel NF-κB
protein expression decrease in MDA-MB-231, a tumorigenic
triple-negative breast cancer cell line. It can be concluded that Dox activated apoptosis by inducing proteolytic processing of Bcl-2 family,
caspases and simultaneously decreased oxidative stress by influencing ROS damage in MCF-7 and MDA-MB-231 cell lines.