Abstract
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 G2/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 G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.
Highlights
Gastric cancer is the fourth most prevalent malignant disease and the second leading cause of cancer‐related mortality worldwide [1,2]
To evaluate the effects of CTD on the proliferation of human gastric cancer cells, MTS assays were used to measure the growth of SGC‐7901 and BGC‐823 cells
The present results revealed that CTD inhibited the proliferation of the SGC‐7901 and BGC‐823 cells in a dose‐ and time‐dependent manner (Fig. 1)
Summary
Gastric cancer is the fourth most prevalent malignant disease and the second leading cause of cancer‐related mortality worldwide [1,2]. Gastric cancer is characterized by a high mortality rate and a short median survival time, since it is too late for. The induction of cell cycle arrest and apoptosis has been demonstrated to induce cancer cell death and may be considered as a strategy to deal with gastric cancer [5]. The cell cycle has been investigated widely and the cyclin‐dependent kinase 1 (CDK1)/cyclin B complex has been found to play a significant role in the regulation of the G2/M phase [6]. Apoptosis is a form of cell death that can be activated through at least two signaling pathways, the caspase‐dependent and caspase‐independent pathways, and several involve the mitochondria and B‐cell lymphoma‐2 (Bcl‐2) family proteins [7]
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