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Cantharidin induces G(2)/M phase arrest and apoptosis in human gastric cancer SGC-7901 and BGC-823 cells

The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular p...

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Detalles Bibliográficos
Autores principales: ZHANG, CHENJING, CHEN, ZHONGTING, ZHOU, XINGLU, XU, WEN, WANG, GANG, TANG, XIAOXIAO, LUO, LAISHENG, TU, JIANGFENG, ZHU, YIMIAO, HU, WEN, XU, XIANG, PAN, WENSHENG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214476/
https://www.ncbi.nlm.nih.gov/pubmed/25364455
http://dx.doi.org/10.3892/ol.2014.2611
Descripción
Sumario:The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G(2)/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G(2)/M phase arrest and cell apoptosis. CTD may induce cellular G(2)/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.