Bortezomib inhibits gastric carcinoma HGC-27 cells through the phospho-Jun N-terminal kinase (p-JNK) pathway in vitro.

The study is designed to explore the anticancer mechanism of Bortezomib. The effects of Bortezomib on the proliferation of human gastric cancer cells HGC-27 and expression levels of the phospho-Jun N-terminal kinase (p-JNK) pathway-related proteins in vitro were investigated. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed that the Bortezomib significantly decreased the viability of HGC-27 cells and induced apoptosis. Western blot showed that the Bortezomib strongly increased the levels of p-JNK, caspase-3, PARP, and bax proteins while it increased the level of bcl-2. However, SP600125 can significantly decrease antitumour effects of Bortezomib in HGC-27 cells. It can be concluded that Bortezomib has significant inhibitory effects on the growth of HGC-27 cells. The effect may be achieved partly via upregulating JNK pathway and its down-stream apoptosis-related proteins. Therefore, Bortezomib may be beneficial in gastric carcinoma treatment.