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From OncoLog, February 2014, Vol. 59, No. 2

Graphic: In Brief

PKM2 Identified as Potential Prognostic Marker for Glioblastoma

Pyruvate kinase M2 (PKM2), a protein kinase known to be overexpressed in solid tumors, has been identified as a critical component of cancer cell division and a possible prognostic marker and therapeutic target for glioblastoma.

In a study led by Zhimin Lu, Ph.D., a professor in the Department of Neuro-Oncology at The University of Texas MD Anderson Cancer Center, researchers found that PKM2 interacts directly with critical cell division machinery and is an essential regulator of glioblastoma cell reproduction. This finding clarified the role of PKM2 in glioblastoma tumorigenesis.

“This new, additional role for PKM2 in cancer development and survival may provide a molecular basis for diagnosing and treating tumors with upregulated PKM2.”
– Dr. Zhimin Lu
PKM2 had been identified as an oncogene owing to its role in tumor metabolism, especially in epidermal growth factor receptor–positive tumors. However, more recent research identified other functions of PKM2. Dr. Lu’s group sought to determine whether PKM2 played a role in mitosis.

Cells go through several checkpoints during mitosis, and one of the most stringent of these is the spindle assembly checkpoint. Spindles are collections of microtubules that help segregate a single copy of each chromosome to each daughter cell by binding to chromosomes. A key component of this binding is the Bub3-Bub1-Blinkin protein complex.

Dr. Lu’s group found that PKM2 phosphorylates Bub3; Bub3 phosphorylation is necessary for the Bub3-Bub1 complex to bind to Blinkin and participate in spindle assembly. The researchers also found that depletion of PKM2 led to defects in cell division and increased rates of apoptosis in multiple cancer cell lines. Dr. Lu said, “Depleting PKM2 led to an uneven distribution of DNA in the two new cells, triggering programmed cell death, or apoptosis, of those cells after division.”

When the researchers analyzed a library of glioblastoma tissue samples, they found that patients whose tumors had the lowest levels of Bub3 phosphorylation (indicating low PKM2 activity) had a significantly longer median survival duration than did patients with the highest levels of Bub3 phosphorylation. This finding indicates that PKM2 protein kinase activity may be a prognostic marker for glioblastoma.

“This new, additional role for PKM2 in cancer development and survival may provide a molecular basis for diagnosing and treating tumors with upregulated PKM2,” Dr. Lu said. The researchers published their findings in January in the journal Molecular Cell.

For more information, talk to your physician, visit www.mdanderson.org, or call askMDAnderson at 877-632-6789.

Other articles in OncoLog, February 2014 issue:

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