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

onsible for the final step of the process. Previous work from the Cantley lab had suggested that inhibition of PKM2 by growth factor signaling was providing a stall-point in the glycolytic process, functioning like a dam in a river to enable glucose breakdown products to accumulate and eventually spur cancer cell growth.

But the investigators thought there might be more to the story.

"Growth factor signaling emerged relatively late in evolution but glycolysis is a highly conserved process and occurs in bacteria much like it occurs in human cells," says Dimitrios Anastasiou, PhD, a Research Fellow in the Department of Signal Transduction at BIDMC and the Department of Systems Biology at HMS and first author of this new paper. "We were intrigued by the possibility that something other than growth factors might also be influencing the activity of PKM2."

They turned their attention to reactive oxygen species (ROS), chemically reactive molecules that form as a natural byproduct of cell metabolism and can lead to cell damage when not kept under control. "To survive, cancer cells require the ability to squelch potentially toxic ROS molecules, which can arise as a result of both their aberrant metabolism as well as their environment," explains Anastasiou. "We thought that PKM2 might somehow be playing a supporting role in tamping down ROS."

To test this hypothesis, the scientific team embarked on a series of experiments that showed ROS can inhibit PKM2 activity, and that low PKM2 activity under oxidative stress helps push glucose into pathways that generate antioxidant molecules.

"We engineered cells to express a PKM2 mutant that is resistant to ROS-induced inhibition," says Anastasiou. "This showed us that, when challenged by oxidative stress, these cells died more readily than cells expressing the wild-type oxidizable version of PKM2. Strikingly, we also observed that oxidation-resistant PKM2 could not efficiently support the
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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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