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

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [1]; ;  [2];  [1];  [2];  [1]
  1. Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu (China)
  2. The Graduate School, Xuzhou Medical College, Xuzhou, Jiangsu (China)

Highlights: Black-Right-Pointing-Pointer The expression levels of Bex2 markedly increased in glioma tissues. Black-Right-Pointing-Pointer Bex2 over-expression promoted cell proliferation, while its down-regulation inhibited cell growth. Black-Right-Pointing-Pointer Bex2 down-regulation promoted cell apoptosis via JNK/c-Jun signaling pathway. -- Abstract: 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.

OSTI ID:
22210306
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 427, Issue 3; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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