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Study identifies an expanded role for PKM2 in helping cancer cells survive
Date:11/3/2011

ability of human lung-cancer cells to form tumors in mice, but that this defect could be rescued by treating mice with an antioxidant in their water."

The team also collaborated with the National Institutes of Health (NIH) Chemical Genomics Center to identify small molecule PKM2 activators, drugs that keep PKM2 active and thereby prevent cancer cells from using glucose to grow and survive. Treatment of cancer cells with these activators kept PKM2 activity at high levels even under oxidative stress. It also sensitized cells to oxidant-induced death similar to the oxidation-resistant mutant.

"This paper demonstrates that oxidants inhibit PKM2 activity," says Cantley. "While moderate ROS levels can influence growth signaling and promote proliferation, too much ROS can cause irreversible damage to cells, and lead to their demise. We propose that expression of PKM2 allows cancer cells greater flexibility in manipulating how glucose is metabolized to ensure that ROS concentrations remain low.

"Now that we've figured out yet another scheme that cancer uses to survive, we might be able to use small molecule PKM2 activators to prevent cancer from inhibiting the enzyme," he adds. "Because radiation therapy and some chemotherapeutic agents are believed to kill cancer cells by inducing excess ROS, there is a possibility that PKM2 activators may improve the efficiency of these therapies."


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Contact: Bonnie Prescott
bprescot@bidmc.harvard.edu
617-667-7306
Beth Israel Deaconess Medical Center
Source:Eurekalert

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