Calreticulin (CRT), a multifunctional protein that regulates varied important cell functions, in addition CRT recently drawn notice that the function of oxidative stress induced apoptosis. At this point, the role of CRT through oxidative stress mediated apoptotic cell death is focused. Herein, we used mammary gland adenocarcinoma cell cells (MCF-7) in vitro to investigate the role CRT overexpression in cell death by promoting ROS induced apoptosis. Human CRT gene was isolated from blood, cDNA was synthesized, CRT was cloned to the XhoI/EcoRI restriction sites of a mammalian expression vector pcDNA 3.1 and plasmid was transfected in to MCF-7 cell line to promote apoptosis. After 24 h and 48 h transfection, cell proliferation, LDH leakage, lipid peroxidation, total protein, and glutathione concentrations were measured. CRT transfected cells expressed higher concentrations of lipid peroxidation and LDH leakage than control MCF -7 cells. There was a significant negative correlation between lipid peroxidation and cell proliferation. Glutathione did not appear to be a significant factor. Therefore, stimulation of CRT may modulate the growth inhibitory effects in human breast cancer cells. One mechanism of growth inhibition may be through increased lipid peroxidation.