Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Sep 1;9(10 Pt 1):3641-4.

Enolase-alpha is frequently down-regulated in non-small cell lung cancer and predicts aggressive biological behavior

Affiliations
  • PMID: 14506152

Enolase-alpha is frequently down-regulated in non-small cell lung cancer and predicts aggressive biological behavior

Yoon Soo Chang et al. Clin Cancer Res. .

Abstract

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.

PubMed Disclaimer

Publication types

LinkOut - more resources