Abstract
Curcumin is a natural compound that appears to be promising for clinical application, as it has been shown in in vitro and in vivo studies to exert antitumor effects by modulating multiple signaling cellular pathways. In the present study, the antitumor effects of curcumin and its mechanism of action were investigated in cultured breast cancer cells. The MTT assay was used to determine the effect of curcumin on breast cancer cell proliferation, flow cytometry was used to detect alterations of the cell cycle, and western blot analysis was used to determine the expression of signaling molecules involved in the cell cycle, proliferation and apoptosis. The results revealed that curcumin significantly inhibited the proliferation of various breast cancer cell lines, such as T47D, MCF7, MDA-MB-231 and MDA-MB-468, with an IC50 at the micromolar level, indicating the potent antitumor activity of curcumin. In-depth study of its mechanism of action revealed that curcumin induced cell cycle arrest at the G2/M phase and decreased the expression of the CDC25 and CDC2 proteins, while increasing the expression of P21. In addition, curcumin inhibited the phosphorylation of protein kinase B (Akt)/mammalian target of rapamycin (mTOR), decreased B-cell lymphoma 2 (BCL2) and promoted BCL-2-associated X protein (BAX) and cleavage of caspase 3, subsequently inducing apoptosis of breast cancer cells. In conclusion, curcumin inhibited the proliferation of breast cancer cells and induced G2/M phase cell cycle arrest and apoptosis, which may be associated with the decrease of CDC25 and CDC2 and increase of P21 protein levels, as well as inhibition of the phosphorylation of Akt/mTOR and induction of the mitochondrial apoptotic pathway. The findings of the present study may provide a basis for the further study of curcumin in the treatment of breast cancer.