Cucurbitacin B Can Inhibit Proliferation,Induce Apoptosis And Autophagy In Breast Cancer

Objective: Breast cancer is a common malignancy in female. What is worse, great number of patients suffering with breast cancer gradually become resistant to chemotherapy. Cucurbitacin B(Cuc B) is documented as a powerful anticancer agent with less toxicity. We try to evaluate the effects of Cuc B on proliferation, migration, apoptosis and autophagy in breast cancer.Methods:Under the condition of 37℃, 5% CO2, we used SRB assay to study the inhibition of 20μM, 50μM, 100μM Cuc B on proliferation in MCF-7 cells for 6h, 12 h and 24 h,respectively. Next, Hoechst 33258 assay was used for detecting the apoptosis of cells after dealing with 20μM, 50μM, 100μM CuB. At last, the potential mochenism of CuB on cell autophagy was assessed by Western blot.Results: Firstly, we can draw a conclusion that Cuc B can significantly inhibit proliferation in a dose and time dependent manner by use of SRB assay. Hoechst 33258 assay results also revealed that 20μM CucB can induce apoptosis and 50μM, 100μM CucB work more powerfully. Western Blotting results implied that CucB induce apoptosis and autophagy by increasing LC3-II/LC3-I, decreasing P62 in MCF-7 cells.Conclusions:1. 20μM, 50μM, 100μM Cuc B dealing with cells for 6h,12 h,24h reveals that 50μM, 100μM Cuc B inhibits the survival rates of MCF-7 cells and functions in a dose and time dependent manner2. Hoechst 33258 assay results also revealed that 20μM CucB can induce changes in cellular morphology, leading to apoptosis. 50μM, 100μM CucB worked more powerfully. 3. Western Blotting results implied that 20μM CucB induce apoptosis and autophagy byincreasing LC3-II/LC3-I, decreasing P62 in MCF-7 cells. The phenomenon was moreobvious in 50μM,100μM CucB.