[Vitexicarpin affects proliferation and apoptosis in mutated p53 breast cancer cell].
Palabras clave
Abstracto
OBJECTIVE
To elucidate the effect of proliferation and apoptosis induced by vitexicarpin in mutated p53 Hs578T cell line and study the expression of c-Myc, p21 and Bcl-2 protein in Hs578T and wild p53 MCF-7 cell pre-treated with vitexicarpin.
METHODS
Cells were treated with various concentrations of vitexicarpin (0, 0.1, 0.2, 0.5, 1.0 micromol/L). MTT assays were used to detect cell proliferation at different time points with different doses of vitexicarpin. TUNEL assays were performed to examine apoptosis in cells pretreated with vitexicarpin. The authors detected three main proteins involved in apoptosis: c-Myc, bcl-2 and p21 protein in various concentrations of vitexicarpin-treated cells. To understand the function of c-Myc protein in the effect of vitexicarpin, the authors transiently transfected c-Myc protein in Hs578T cell and detected the cellular effect of vitexicarpin.
RESULTS
Proliferation of Hs578T and MCF-7 cells were inhibited markedly by vitexicarpin at concentrations above 0.2 micromol/L (IC50 = 0.25 micromol/L and 0.53 micromol/L at 72 h respectively). TUNEL assays revealed that the rates of TUNEL positive cells were 10.15%, 27.33% and 35.34% when exposing Hs578T cells to 0.1, 0.2 and 0.5 micromol/L of vitexicarpin respectively. In control cells, the rates of TUNEL positive cells were 4.65%. Cells pretreated with higher concentrations of vitexicarpin expressed less c-Myc and Bcl-2 in Hs578T cells.In contrast, p21 decreased when cells were treated with the same conditions. When c-Myc transient transfection was performed in vitexicarpin-treated cells, the effect of p21 and Bcl-2 disappeared. The proliferative function of vitexicarpin declined in Hs578T/c-Myc cells. When treated with 0.5 micromol/L vitexicarpin, A value increased 1.53 times at 72 h. Conversely, A value decreased 48% at the same condition in MCF-7/c-Myc cells.
CONCLUSIONS
The suppressing mechanism of vitexicarpin for malignant tumors is through c-Myc in p53 mutated Hs578T cells. And it is multi-directional and varies in different cells.
