Abstract
Curcumin is the major component of the spice turmeric, extracted from the rhizomes of the plant Curcuma longa. It exerts a number of therapeutic effects, including the inhibition of cancer cell proliferation. However, the anti-carcinogenic mechanism of curcumin has not been fully elucidated. Triple-negative breast cancer (TNBC), which lacks expression of the estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/EGFR2), is an aggressive breast cancer phenotype with a poor prognosis. In this study, we investigated the effects of curcumin on triple-negative breast cancer cells and the possible molecular mechanisms. The MDA-MB-231 TNBC cells were treated with curcumin, the growth inhibition ratio of the cells was measured by MTT assay, apoptosis was detected by flow cytometry and the expression levels of extracellular regulated protein kinase (ERK1/2), pERK1/2, EGFR and pEGFR were detected by western blotting. After treatment with different concentrations of curcumin, the growth inhibition rates of the MDA-MB-231 breast cancer cells of the 30 µmol/ml curcumin-treated group were significantly different from those of the other groups. The level of apoptosis of the curcumin-treated group (26.34%) was significantly different from that of the control group (2.76%). The expression levels of pERK1/2 and pEGFR in the curcumin-treated group were significantly decreased compared with those of the control group. These results indicate that curcumin is able to inhibit the proliferation of TNBC cells. Inhibition of the EGFR signaling pathway is the likely underlying molecular mechanism.
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