Abstract
Objective To explore the effects of parthenolide on growth inhibition, cell aoptosis and molecular mechanism of human 786-O kidney cancer cells. Methods The inhibitory effect of parthenolide on human786-O cells was determined by MTT assay.The cell apoptosis and the cell cycle were analyzed by flow cytometry.Bax and the gene change of Bax and Bcl-2 were analyzed by fluorescence quantitative PCR, Bax and Bcl-2 family proteins were analyzed by Westerm blot. Results Parthenolide inhibited the proliferation of 786-O cells in a dose-dependent and time-dependent manner.As showed by flow cytometry, parthenolide treatment of the 786-O cells led to significant G1-phase cell cycle arrest in a dose-dependent manner and a decrease in cell population in the S-phase, whereas the population of cells in G2/M phase did not chang significantly.Flow cytometIy also showed a dose-dependent increase in 786-O cells apoptosis by parthenolide treatment.Westem blot analysis indicated a down-regulation of phosphorylated CyclinDl in a dose-dependent manner in 786-O cells by parthenolide treatment.In the gene and protein level, parthenolide treatment to 786-O cell lines resulted a significant reduction in Bcl-2 expression but an increase in Bax protein in a dose-dependent manner. Conclusions Parthenolide treatment can 1ead to a significant dose-dependent and time-dependent inhibition in the growth and an increase in apoptosis of human 786-O Kidney cancer cells.The mechanism of action of parthenolide may be related to inhibition of CyclinDl activation and regulation of Bcl-2 and Bax expression in human 786-O Kidney cancer cells. Key words: Kidney Neoplasms; Tanacetum parthenium; Cell Proliferation; Apoptosis; Cell Cycle
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