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

• Human gastric cancer cells HGC-27
• Bortezomib decreased the viability of HGC-27 cells and induced apoptosis.
• Bortezomib increased the levels of p-JNK, caspase-3, PARP, and bax proteins.
• Bortezomib inhibitory effects on the growth of HGC-27 cells
• Bortezomib may be beneficial in gastric carcinoma treatment.

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.