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Metabolic protein plays unexpected role in tumor cell formation and growth
Date:11/6/2011

ression, which are essential for tumor formation, are conventionally thought to be regulated primarily by distinct signaling complexes," Lu said. The new findings integrate the two major mechanisms for regulating cancer cell growth by a key metabolic enzyme. "These two important regulatory processes are under the control of pyruvate kinase M2."

New insight into brain malignancies and cancer therapy

Beta-catenin activation that is independent of the Wnt signaling pathway have been observed in many types of cancer. This study reveals a critical mechanism underlying Wnt-independent beta-catenin activation and indicates that c-Src-phosphorylated beta-catenin and nuclear PKM2 are independent predictors of glioma malignancy.

The researchers analyzed brain tumors in 84 patients who had been treated with radiation and chemotherapy after surgery. Those who had low beta-catenin Y333 phosphorylation or low expression of PKM2 in the nucleus (28 cases each) had a median survival of 185 weeks and 130 weeks, respectively.

Median survival decreased for those who had high levels of beta-catenin phosphorylation or nuclear PKM2 expression (56 cases each) to 69.4 weeks and 82.5 weeks, respectively.

Findings include:

  • PKM2-dependent beta-catenin activation is instrumental in EGFR-promoted tumor cell proliferation and brain tumor development.
  • c-Src activity, beta-catenin Y333 phosphorylation, and PKM2 nuclear accumulation are positively correlated in human glioblastoma specimens.
  • Levels of beta-catenin phosphorylation and nuclear PKM2 are correlated with grades of glioma malignancy and prognosis.

Personalized therapy with Src inhibitors

One potential implication of their research is the potential use of c-Src-dependent beta-catenin Y333 phosphorylation levels as a biomarker for selecting patients for treatment.

"This finding is very important because EGFR-based therapy i
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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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