X Y Liu1, T H Lv, X D Xie, J Li, G Su, H Wu. 1. School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu Province, China.
Abstract
OBJECTIVE: To investigate the effects and mechanisms of sesquiterpene (+)-chabranol on proliferation of a panel of four human tumour cell lines (BGC-823, SGC-7901, SSMC-7721 and HepG2). METHODS: Cell viability was assessed using a standard methyltetrazolium assay; cell-cycle analysis of BGC-823 cells was performed by flow cytometry. Transmission electron microscopy (TEM) was used to examine the ultrastructure of BGC-823 cells exposed to (+)-chabranol. Apoptosis was investigated by evaluating DNA laddering, using gel electrophoresis. RESULTS: (+)-Chabranol had a marked time- and concentration-dependent inhibitory effect on BGC-823 cell proliferation. The effect was less marked in SGC-7901, SSMC-7721 and HepG2 cells. Exposure of BGC-823 cells to (+)-chabranol arrested the cell cycle at G(1). Evidence of apoptosis and autophagy was observed by TEM; DNA laddering in BGC-823 cells supported the presence of apoptosis. CONCLUSIONS: This study suggested that (+)-chabranol has antitumour activity against BGC-823 cells, and may exert its action by inhibition of proliferation and induction of apoptosis and autophagy. With further development, (+)-chabranol may represent a potential novel treatment for poorly differentiated gastric cancer.
OBJECTIVE: To investigate the effects and mechanisms of sesquiterpene(+)-chabranol on proliferation of a panel of four humantumour cell lines (BGC-823, SGC-7901, SSMC-7721 and HepG2). METHODS: Cell viability was assessed using a standard methyltetrazolium assay; cell-cycle analysis of BGC-823 cells was performed by flow cytometry. Transmission electron microscopy (TEM) was used to examine the ultrastructure of BGC-823 cells exposed to (+)-chabranol. Apoptosis was investigated by evaluating DNA laddering, using gel electrophoresis. RESULTS:(+)-Chabranol had a marked time- and concentration-dependent inhibitory effect on BGC-823 cell proliferation. The effect was less marked in SGC-7901, SSMC-7721 and HepG2 cells. Exposure of BGC-823 cells to (+)-chabranol arrested the cell cycle at G(1). Evidence of apoptosis and autophagy was observed by TEM; DNA laddering in BGC-823 cells supported the presence of apoptosis. CONCLUSIONS: This study suggested that (+)-chabranol has antitumour activity against BGC-823 cells, and may exert its action by inhibition of proliferation and induction of apoptosis and autophagy. With further development, (+)-chabranol may represent a potential novel treatment for poorly differentiated gastric cancer.