Effects of catechin, diclofenac and celecoxib on the proliferation of MCF-7 and LTED MCF-7 cells

Breast cancer is common among women especially after menopause. Inflammation is now considered as a risk factor of cancer and cyclooxygenase-2 (COX-2) enzymes are highly expressed in many cancers. COX-2 is the inducible enzyme responsible for the synthesis of pro-inflammatory prostaglandins. There are evidences that COX inhibitors especially those which inhibit COX-2 have a role in the management of cancers. Since breast tumors are generally estrogen sensitive, whether or not their response to COX inhibitors is changed when they are under the condition of estrogen deprivation. This in vitro study aimed to investigate the effects of different COX inhibitors, i.e. catechin − selective COX-1 inhibitor, diclofenac − COX-1/COX-2 inhibitor, and celecoxib − selective COX-2 inhibitor, at concentrations of 10−10–10−4 M on the proliferation of MCF-7 cells and long-term estrogen-deprived (LTED) MCF-7 cells. The effects of these COX inhibitors were assessed on day 2 and day 6 of incubation using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) method. Morphological features of these cells on day 2 of incubation with COX inhibitors were visualized after Ho33342 staining and apoptosis was confirmed by DNA fragmentation. The results indicated that diclofenac and celecoxib, but not catechin, at high concentrations could effectively inhibit the proliferation of both cell types. Celecoxib was, however, the only drug used in this study that could markedly induce DNA fragmentation in LTED MCF-7 cells at the highest concentration (10−4 M). This study provides the in vitro evidence to support the beneficial effect of COX-2 inhibitors against breast tumors whether or not at the estrogen-deprived stage.