Purpose: To evaluate the effect on breast cancer cell proliferation and apoptosis after silencing the HCCR-1 and to study its mechanism.
Methods: HCCR-1 siRNA was transfected into the breast cancer cell line MCF -7, and mRNA and protein level of HCCR-1 and Bax were evaluated by real-time quatitative PCR (qRT-PCR) and Western blotting, respectively. The cell proliferation and apoptosis were studied by MTT assay and flow cytometry.
Results: The apoptosis rate in the experimental, control and blank groups were 32.57±2.35%, 3.53±0.60% and 3.15±0.46% respectively. The apoptosis rate of MCF-7 cells was significantly increased in the experimental group, compared with the other two groups (p<0.05). The A490 value in the experimental, control and blank groups were: 24h: 0.78±0.06, 1.18±0.05, 1.24±0.05; 48h: 1.09±0.05, 1.48±0.02, 1.54±0.04; 72h: 1.29±0.01, 1.81±0.02, 1.84±0.04. The proliferation of MCF-7 cells was significantly decreased in the experimental group, compared with the other two groups (p<0.05). The mRNA levels of HCCR-1 and Bax in the experimental, control and blank groups were: HCCR-1 0.46±0.03, 1.01±0.11, 1.00; and Bax 4.40±0.99, 1.03±0.10, 1.00. The protein levels were: HCCR-1 0.62±0.07, 0.89±0.09, 0.94±0.17; and Bax 0.95±0.22, 0.67±0.19, 0.69±0.11. The expressions of mRNA and protein of HCCR-1 were significantly reduced, however the expressions of mRNA and protein of Bax were significantly increased in the experimental group compared with the other two groups (p<0.05).
Conclusions: HCCR-1 siRNA transfection causes significant increase in the apoptosis and decreases in the proliferation of MCF-7 cells．These effects are related to the upregulation of the Bax expression in the MCF-7 cells.