Abstract
The aim of the present study was to elucidate the anticancer effect of pachymic acid (PA) in gastric cancer SGC-7901 cells and the potential molecular mechanisms involved. Cell Count kit-8 assay was performed to examine the effect of PA on the cell proliferation of SGC-7901 cells. Cell cycle, cell apoptosis, mitochondria membrane potential (Dψm) and reactive oxygen species (ROS) analysis were assessed by flow cytometry, respectively. DNA fragmentation assay was performed by Hoechst 33258 staining. Western blotting was performed to detect the effect of various concentrations of PA on the levels of BCL2 associated X protein (Bax) expression as well as B-cell lymphoma 2 (Bcl-2), cytochrome C (cyt-c) and caspase-3 in SGC-7901 cells. It was demonstrated that PA was able to significantly inhibit the viability and induce G0/G1 cell cycle arrest of SGC-7901 cells in a concentration-dependent manner. The apoptotic rate and ROS generation were markedly increased, while Dψm was decreased following the treatment of SGC-7901 cells with various concentrations of PA. Moreover, the expression of Bax, cytochrome c and caspase-3 were markedly increased and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) was significantly inactivated and BCL-2 expression was decreased following PA treatment in SGC-7901 cells. Notably, JAK2 inhibitor (AG490) mimics the effects of PA on the viability and apoptosis of SGC-7901 cells. Further in vivo study indicated that treatment with PA significantly inhibited the growth of tumor in nude mice that were transplanted with SGC-7901 cells in a concentration-dependent manner. These results may advance the current understanding of the anticancer mechanisms of PA in gastric cancer.