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The Role of Hydrogen Peroxide as an Endogenous Growth Factor in Human Breast Cancer Cells

Recently a significant number of studies have reported the role of ROS in the progression of a variety of cancers including breast cancer. In this study we have assessed the levels of O2− and H2O2 in a panel of breast cancer cells comprising both estrogen receptor positive and negative cell lines and compared them with those of normal human breast epithelial cells. We have established a significant role of H2O2 in breast cancer survival and proliferation by either silencing or overexpressing catalase in a breast cancer cell line, MDA‐MB‐468. We observed that silencing of catalase was accompanied by an increase in H2O2 production accompanied by an increase in proliferation rate. This was associated with an increase in the phosphorylation status of ERK1/2 and AKT along with a decrease in PP2A (protein phosphatase 2A) activity. Conversely over expression of catalase in MDA‐MB‐468 caused a significant reduction in H2O2 production resulting in apoptosis with a decrease in phosphorylation of ERK1/2 and AKT along with an increase in PP2A activity. This strongly indicated the role of H2O2 as an endogenous growth factor in breast cancer cells. We further established this fact by obtaining similar results by overexpressing GPX1(glutathione peroxidase1) another H2O2 scavenging enzyme. Interestingly overexpression of catalase did not result in apoptosis in normal human mammary epithelial cells attributing this phenomenon specifically to cancer cells, lending a significant therapeutic potential to the findings.