A new copper complex enhanced apoptosis in human breast cancerous cells without considerable effects on normal cells

Complexes with copper ions have attracted a lot of attention for cancer therapy, because it's assumed that the endogenous metals may be less toxic for healthy cells than cancerous cells. In the previous study, we observed the [Cu(L)(phen)] compound indicated an inhibiting effect on the MCF7 cells with low side effects on normal cells. In this research, we aim at examining the molecular system engaged in the induction of apoptosis in L929 and MCF7 cells after being treated with the [cu(L)(phen)] compound. The expressing of a number of apoptotic genes, such as bcl-2, caspase-8, p53, bax as well as bid were evaluated by RT-PCR following 48- and 24-hour treatments by the [cu(L)(phen)] compound at the concentrations of IC50. Cleavage and fragmentation of DNA were observed in MCF-7 treated cells. In addition, after the treatment of cells by this complex, bcl-2 expression decreased significantly at MCF7 cells; however, it was not significantly changed at the cells of L929. The expression of bax, caspase8, p53 and bid genes was significantly increased in both MCF-7 and L929 cells. Due to the increase in the bax/bcl-2 ratio as well as the increase in caspase8 and bid genes expression in MCF7 cells after the treatment, it can be concluded that this complex activates apoptosis from intrinsic and extrinsic apoptotic routes in malignant cells. However, due to the lack of significant changes in bax/bcl-2 ratio at cells (L929) and the increase in the caspase8 and bid genes expression, this complex mainly activates apoptosis through the only extrinsic apoptotic pathway in normal cells.