Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway

The function of Bex2, a member of the Brain Expressed X-linked gene family, in glioma is controversial and its mechanism is largely unknown. We report here that Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase (JNK) pathway. The expression level of Bex2 is markedly increased in glioma tissues. We observed that Bex2 over-expression promotes cell proliferation, while down-regulation of Bex2 inhibits cell growth. Furthermore, Bex2 down-regulation promotes cell apoptosis and activates the JNK pathway; these effects were abolished by administration of the JNK specific inhibitor, SP600125. Thus, Bex2 may be an important player during the development of glioma.

► The expression levels of Bex2 markedly increased in glioma tissues.
► Bex2 over-expression promoted cell proliferation, while its down-regulation inhibited cell growth.
► Bex2 down-regulation promoted cell apoptosis via JNK/c-Jun signaling pathway.