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"We've shown that if you disrupt this interaction - if you block the binding of these two proteins - the tumor cells are more prone to being killed," he said.

UF researchers identified FAK's interaction with VEGFR-3 in cell cultures of human breast cancer. Breast cancers that pump out high volumes of FAK and VEGFR-3 are more aggressive tumors, Cance said. The scientists were able to block FAK from binding with VEGFR-3 by introducing a different protein that stopped cancer cells from dividing and caused them to die but spared normal breast cells.

"FAK is a critical molecule, and in the future different ways of targeting either the enzyme itself or targeting the binding between these various proteins will have a major impact on cancer, I believe," Cance said. "We think it's one of the Achilles' heels for tumor cells and you can disrupt it in a number of different ways. For example, we might be able to design drugs that mimic this area of binding and disrupt it in patients."

Because normal cells generate much lower levels of FAK than tumor cells do, treatments could be developed to target FAK and VEGFR-3 at dosages markedly less toxic to healthy tissues yet lethal to cancer.

"We have a therapeutic window," said Cance, the study's senior investigator. "In normal cells we've shown you can knock it out and cells can still resist the loss of expression of focal adhesion kinase, whereas the tumor cells use it as one of their major proteins for survival."

UF surgical resident Christopher Garces, M.D., and UF research assistant professors Elena Kurenova, Ph.D., and Vita Golubovskaya, Ph.D., also were involved in the work
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Source:University of Florida