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An Achilles heel in cancer cells
Date:12/8/2008

ie. Akt could not protect cells from this form of apoptosis and, indeed, because Akt impaired the normal ROS scavenging in the cell, hyperactive Akt actually had the effect of making the cells more vulnerable to these ROS inducers. This enabled selective killing of cancer cells, expressing hyperactive Akt, and not normal cells.

The researchers also devised another strategy to exploit Akt's Achilles heel to successfully target and kill cancer cells.

An FDA-approved chemotherapy drug called rapamycin can be used to arrest cell tumor growth. A drawback of this drug is that it doesn't kill the cells, it just arrests the growth of the tumor. When the drug is removed the tumor may grow again.

"Rapamycin's other drawback is complicated feedback regulation that we turn to our advantage," Hay said. "It turns out rapamycin's target and Akt talk to each other in the cell." If the rapamycin target is hyperactive, Akt is inhibited, and if Akt is active, the rapamycin target is activated.

"So even though cancer cells treated with rapamycin stop dividing, they activate Akt, which makes the cells more resistant to other chemotherapy drugs," said Hay. "But we use that to our advantage. Because overactivation of Akt sensitizes the cells to ROS mediated cell death, if we treat the cells with ROS inducers and rapamycin together we can now kill the cells, not just arrest their growth."

The new study "provides a proof of the principle that Akt's Achilles heel -- a consequence of its role in metabolism -- can be exploited in at least these two ways to selectively target and kill cancer cells," Hay said.


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Contact: Jeanne Galatzer-Levy
jgala@uic.edu
312-996-1583
University of Illinois at Chicago
Source:Eurekalert

Page: 1 2

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