Abstract: Objective To investigate whether calpain is involved in epidermal growth factor (EGF)-enhanced colony formation in estrogen receptor (ER) negative breast cancer cells. Methods ER-negative MDA-MB-231 breast cancer cells were employed as a model system, Western lot analysis was used to observe protein alterations. Colony formation assay applied to evaluate the role of calpain in EGF-stimulated cell growth. Calpain specific inhibitor, calpeptin (Calp), was employed for pre-treatment of cells to observe its effect on the EGF actions. Results (1) EGF induced over-expression and truncation of FAK (also of cyclin E) protein in MDA-MB-231 breast cancer cells（p<0.01）; (2) EGF-enhanced processing of FAK could be blocked by calpeptin（p<0.05）; (3) EGF induced calpain 1 autolysis and this effect could be tremendously suppressed by pre-treatment with calpeptin（p<0.05）, and (4) Calpeptin greatly inhibited EGF-enhanced cell growth（p<0.05）. Conclusion Calpain is possibly a potential target for the treatment of ER-negative breast cancer.

Key words: Key words： Epidermal growth factor, Calpain, estrogen receptor, cell growth, Breast cancer