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Journal of Cancer Research and Clinical Oncology

Published in:

01-02-2010 | Original Paper

Glycolytic phenotype in breast cancer: activation of Akt, up-regulation of GLUT1, TKTL1 and down-regulation of M2PK

Authors: Melanie Schmidt, Hans-Ullrich Voelker, Michaela Kapp, Mathias Krockenberger, Johannes Dietl, Ulrike Kammerer

Published in: Journal of Cancer Research and Clinical Oncology | Issue 2/2010

Abstract

Purpose

Metabolic dependence on glucose utilisation has been described for different tumours characterised by activation of Akt, upregulation of GLUT1, M2PK and TKTL1. To date, however, little is known about glucose metabolism in breast cancer tissue.

Methods

We analysed 55 breast cancer specimens, 26 adjacent ductal carcinomas in situ (DCIS) and 23 adjacent normal breast tissues for expression of glycolytic markers by immunohistochemistry.

Results

We found expression of pAkt in 49%, GLUT1 in 25%, M2PK in 68% and TKTL1 in 31% of the tumours investigated. Expression of pAkt and Her2neu are positively correlated with borderline significance (P = 0.055). Expression of pAkt, GLUT1 and TKTL1 were higher in breast cancer and DCIS than in normal tissue. Surprisingly, M2PK expression was highest in normal breast tissue.

Conclusions

We found a glycolytic phenotype in a high percentage of breast cancer samples. Inhibition of glycolysis might evolve as a future option for breast cancer therapy.

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Title: Glycolytic phenotype in breast cancer: activation of Akt, up-regulation of GLUT1, TKTL1 and down-regulation of M2PK
Authors: Melanie Schmidt
Hans-Ullrich Voelker
Michaela Kapp
Mathias Krockenberger
Johannes Dietl
Ulrike Kammerer
Publication date: 01-02-2010
Publisher: Springer-Verlag
Published in: Journal of Cancer Research and Clinical Oncology / Issue 2/2010
Print ISSN: 0171-5216
Electronic ISSN: 1432-1335
DOI: https://doi.org/10.1007/s00432-009-0652-y

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Abstract

Purpose

Methods

Results

Conclusions

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