EFFECT OF SAHA ON PROLIFERATION OF BREAST CANCER CELLS BY ACTIVATING THE INTRACELLULAR APOPTOSIS PATHWAY

Hanyang Tao¹, Sandi Shen², Ningdong Hu^{2, *}

¹Guangzhou Medical University, Guangzhou, PR China - ²Department of Cardiothoracic Surgery, The Sixth Affiliate Hospital of Guangzhou Medical University, Qingyuan, PR China

Objective: To explore the effect of the molecular-targeted drug suberoylanilide hydroxamic acid (SAHA) on the proliferation of breast cancer cells, especially through activating apoptotic pathways in cancer cells. 

Methods: The breast cancer cell line MCF-7 was monitored under treatment with different doses of SAHA. There were five dosage groups established: the control group (0μml/L SAHA), 2.5μml/L SAHA, 5μml/L SAHA, 10μml/L SAHA, and 20μml/L SAHA. The effective range of each SAHA dose was determined, the effect of SAHA on the proliferation and migration of MCF-7 cells in each group was analysed, and its effect on the proliferation and migration of breast cancer cells through the apoptotic pathway was investigated. 

Results: In the dose range of 0μml/L to 20μml/L, the levels of histone H4 acetylation in the SAHA-dosed groups were significantly higher than in the control group (P<0.05) and was dose-dependent. The relative cell survival rates and the cell clone formation rates in the SAHA-dosed groups were markedly lower than the rates for the control group (P<0.05); this was dose dependent. Cell migration in the SAHA-dosed groups was dramatically lower than in the control group (P<0.05); this was dose dependent. The expression of BAX and Caspase-3 in the SAHA-dosed groups was remarkably higher than in the control group, and the expression of the Bcl-2 protein was significantly lower than in the control group (P<0.05). 

Conclusion: Treatment with SAHA can inhibit the proliferation and migration of cancer cells by activating the intracellular apoptosis pathway; the cancer-cell-proliferation-inhibition mechanism may be enacted by decreasing the expression of Bcl-2 proteins and increasing the expression of BAX and Caspase-3 proteins.