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IBA Publikation


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IBA Publikation
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IBA Publikation

Isotype-specific inhibitors of the glycolytic key regulator pyruvate kinase subtype M2 moderately decelerate tumor cell proliferation

    Gilles Spoden, Sybille Mazurek, Dieter Morandell, Nicole Bacher, Michael Ausserlechner, Pidder Jansen-Dürr, Erich Eigenbrodt, Werner Zwerschke

IBA Publikation, pp. 312-231, 2008/09/01

doi: 10.1002/ijc.23512


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doi:10.1002/ijc.23512

Abstract

Reprogramming of carbohydrate metabolism is a hallmark of tumor cells which have a high demand of energy as well as of precursors for DNA synthesis and other biosynthetic processes to grow and survive. Such cells preferentially utilize the glycolytic pathway to achieve these demands. The important role of glycolysis for tumorigenesis is underlined by studies providing evidence for a direct link between cancer genes and the reprogramming of this pathway. Thus, several oncoproteins have been shown to target glycolytic enzymes. One important target is pyruvate kinase isoenzyme M2 (M2-PK), which is directly targeted by the high-risk human papillomavirus type-16 E7 oncoprotein. M2-PK regulates the rate limiting step at the end of the glycolytic pathway in tumor cells. The aim of the present study was to investigate whether specific inhibitors of M2-PK are able to effect tumor cell proliferation and apoptosis. To do this we designed specific inhibitors of M2-PK by molecular engineering of M2-PK-binding peptide aptamers. We demonstrate that these combinatorial proteins specifically bind to M2-PK, block its enzymatic activity and inhibit tumor cell proliferation. Thus, here we rationally developed the first isotype-specific inhibitors of M2-PK, a glycolytic key regulator in tumor cells, and demonstrated that a selective intervention in the fine regulation of M2-PK may interfere with tumor cell proliferation.

Keywords: Tumor Metabolism Peptide Aptamer Proliferation Pyruvate kinase