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Selective inhibition of BMK1 suppresses tumor growth
Date:9/13/2010

A study describing a newly developed pharmacological inhibitor is providing detailed insight into how an enzyme that has been implicated in multiple human malignancies regulates a known tumor suppressor. The research, published by Cell Press in the September 14th issue of the journal Cancer Cell, may have broad application for treating human cancers.

Mitogen-activated protein kinases (MAPKs) are enzymes that regulate multiple cellular activities, including proliferation and cell survival. Mutations in MAPK signaling pathways have been shown to play a significant role in many types of cancer. Of the four different MAPKs that have been identified in mammalian cells, ERK1/2 and BMK1 exhibit significant structural similarity. In fact, recent research has shown that some pharmacological compounds which have been considered to be specific inhibitors of ERK1/2, also interfere with the lesser known BMK1.

"It is critical that results using the common MAPK inhibitors be reevaluated using more specific inhibitors of the BMK1 and ERK1/2 cascades. However, so far there has been no specific small-molecule inhibitor of BMK1 that is effective both in cells and animals," explains senior study author, Dr. Jiing-Dwan Lee, from The Scripps Research Institute in La Jolla, California. "More importantly, the lack of this kind of BMK1 inhibitor has hampered the understanding of the physiological/pathological roles of BMK1."

Dr. Lee and colleagues discovered that promyelocytic leukemia protein (PML), which is a known tumor suppressor, is inhibited by BMK1. "Previous reports had implicated ERK1/2 in the regulation of PML," says Dr. Lee. "However, in our study we found that that BMK1 interacts with PML and suppresses its antitumor actions." To further investigate the BMK1-PML interaction, the researchers developed a compound called XMD8-92 that was remarkably selective at inhibiting BMK1.

Treatment with XMD8-92 blocked tumor cell proliferation
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Contact: Cathleen Genova
cgenova@cell.com
617-397-2802
Cell Press
Source:Eurekalert

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