Targeting DUSPs in glioblastomas – wielding a double-edged sword?
Article first published online: 18 NOV 2013
© 2013 International Federation for Cell Biology
Cell Biology International
Volume 38, Issue 2, pages 145–153, February 2014
How to Cite
Prabhakar, S., Asuthkar, S., Lee, W., Chigurupati, S., Zakharian, E., Tsung, A. J. and Velpula, K. K. (2014), Targeting DUSPs in glioblastomas – wielding a double-edged sword?. Cell Biology International, 38: 145–153. doi: 10.1002/cbin.10201
- Issue published online: 15 JAN 2014
- Article first published online: 18 NOV 2013
- Accepted manuscript online: 23 OCT 2013 01:22PM EST
- Manuscript Accepted: 4 OCT 2013
- Manuscript Received: 26 JUL 2013
- brain/nervous system;
- tumor suppressor
Several dual-specificity phosphatases (DUSPs) that play key roles in the direct or indirect inactivation of different MAP kinases (MAPKs) have been implicated in human cancers over the past decade. This has led to a growing interest in identifying DUSPs and their specific inhibitors for further testing and validation as therapeutic targets in human cancers. However, the lack of understanding of the complex regulatory mechanisms and cross-talks between MAPK signaling pathways, combined with the fact that DUSPs can act as a double-edged sword in cancer progression, calls for a more careful and thorough investigation. Among the various types of brain cancer, glioblastoma multiforme (GBM) is notorious for its aggressiveness and resistance to current treatment modalities. This has led to the search for new molecular targets, particularly those involving various signaling pathways. DUSPs appear to be a promising target, but much more information on DUSP targets and their effects on GBM is needed before potential therapies can be developed, tested, and validated. This review identifies and summarize the specific roles of DUSP1, DUSP4, DUSP6 and DUSP26 that have been implicated in GBM.