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Clinical Cancer Research Vol. 9, 3641-3644, September 1, 2003
© 2003 American Association for Cancer Research


Molecular Oncology, Markers, Clinical Correlates

Enolase-{alpha} Is Frequently Down-Regulated in Non-Small Cell Lung Cancer and Predicts Aggressive Biological Behavior1

Yoon Soo Chang, Weiguo Wu, Garrett Walsh, Waun Ki Hong and Li Mao2

Molecular Biology Laboratory, Department of Thoracic/Head and Neck Medical Oncology [Y. S. C., W. W., W. K. H., L. M.] and Department of Thoracic and Cardiovascular Surgery [G. W.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas, 77030

Purpose: Enolase-{alpha} is a cytoplasmic glycolytic enzyme important in the formation of phosphoenolpyruvate. Enolase-{alpha} and c-myc binding protein (MBP-1) originate from a single gene through alternative use of translational starting sites. Both enolase-{alpha} and MBP-1 can bind to the P2 element in the c-myc promoter and compete with TATA-box binding protein (TBP) to suppress transcription of c-myc.

Experimental Design: To determine a potential role of enolase-{alpha} in vivo, we analyzed enolase-{alpha} expression in non-small cell lung cancer (NSCLC) tissues from 46 patients by Western blotting and immunohistochemical analysis.

Results: Twelve (26%) of the 46 tumors showed a significantly reduced enolase-{alpha} expression. Although no statistically significant association was observed between the down-regulation of enolase-{alpha} and pathological stage, tumor histology, or differentiation, the patients whose tumors showed reduced enolase-{alpha} expression had a significantly poorer overall survival compared with those without down-regulation of this molecule (P = 0.0398).

Conclusions: Our results indicate down-regulation of enolase-{alpha} is common in NSCLC and may play an important role in lung tumorigenesis.




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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2003 by the American Association for Cancer Research.