New use for a cell toxin found to inhibit survival proteins in cancer cells

to look at how the proteins interact with everything else in the cell. By over expressing this protein, the cell is changed in some interesting ways. It creates a situation where the cell becomes dependent upon the protein, he said. Cancers can become addicted to certain proteins, so just by over expressing the protein the cell changes so that it cant live without that protein.

The next step in this research is to use the assays his lab developed to cast a wider net to find additional compounds that have similar properties to 2-Methoxy antimycin, Hockenbery said. This strategy has already yielded one additional Bcl-xL inhibitor with "gain of function" activity, reported in the Molecular Cancer Therapeutics paper. Funding for the study, 2-Methoxy antimycin reveals a unique mechanism for Bcl-xL inhibition, came from the New Technology Development Fund administered by the Hutchinson Center. Additional key investigators in Hockenberys lab included Michael Manion, Ph.D., and Pam Schwartz, Ph.D., and John Fry.


Contact: Dean Forbes
Fred Hutchinson Cancer Research Center

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