【Abstract】ObjectiveTo explore the effect of hepatocyte growth factor/scatter factor (HGF/SF) on apoptosis of colorectal cancer cells induced with curcumin. MethodsMTT assay was used to evaluate the cytotoxicity of curcumin to colorectal cancer cells. Flow cytometry was used to detect the antiapoptosis effect of HGF. ResultsFlow cytometry showed only 64 μg/ml curcumin could play the proliferationinhibiting role in Caco-2 cells leading to their apoptosis; at the same time, different concentrations of HGF could antagonize this inhibitory effect resulting in the decrease of apoptosis, but HGF worked without a concentration-dependent manner. The study on MAPK pathway showed that the protective effect of HGF on the apoptosis of Caco-2 cells was not influenced by inhibiting p42/p44 MAPK and p38 MAPK pathway. ConclusionHGF/SF antagonizes the apoptosis of Caco-2 cells induced with curcumin, but MAPK signaling pathway might not participate in this process.
Objective To investigate the effect of quercetin on human breast cancer cells and related mechanism. MethodsHuman breast cancer cell line MDA-MB-435S was treated by different concentrations of quercetin (12.5, 25, 50, 100 and 200 μmol/L). The inhibition ratio of human breast cancer cell was measured by trypan blue dye exclusion test, the proliferation cycle of human breast cancer cell was analyzed by flow cytometry and the expression of caspase-3 mRNA was determined by RT-PCR. ResultsQuercetin could inhibit the proliferation of breast cancer cell in the dose- and time-dependent manner. Quercetin could change the cell cycle of breast cancer cell, with the concentrations of quercetin increasing, the percentages of breast cancer cell at G0/G1 phase decreased, which increased at S phase, and increased at G2/M phase followed decrease. Quercetin could activate the expression of caspase-3 mRNA in breast cancer cell. ConclusionQuercetin can inhibit proliferation and induce apoptosis of human breast cancer cell, the mechanism may be associated with the change of cell cycle and the upregulation of caspase-3 expression.