Research Article

A Variant of the alpha-methyl-acyl-CoA racemase gene created by a deletion in exon 5 and its expression in prostate cancer

  1. James N. Mubiru1,
  2. Anthony J. Valente2,
  3. Dean A. Troyer1,*

Article first published online: 2 MAY 2005

DOI: 10.1002/pros.20277

Issue

The Prostate

The Prostate

Volume 65, Issue 2, pages 117–123, 1 October 2005

Additional Information

How to Cite

Mubiru, J. N., Valente, A. J. and Troyer, D. A. (2005), A Variant of the alpha-methyl-acyl-CoA racemase gene created by a deletion in exon 5 and its expression in prostate cancer. The Prostate, 65: 117–123. doi: 10.1002/pros.20277

Author Information

  1. 1

    Department of Pathology, the University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas

  2. 2

    Department of Medicine, the University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas

*Department of Pathology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900.

Publication History

  1. Issue published online: 18 AUG 2005
  2. Article first published online: 2 MAY 2005
  3. Manuscript Accepted: 23 MAR 2005
  4. Manuscript Received: 21 FEB 2005

Funded by

  • The National Cancer Institute. Grant Number: 2U01CA086402
  • San Antonio Center-Biomarkers for Prostate Cancer
  • Early Detection Research Network

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Keywords:

  • prostate cancer;
  • alternative splicing;
  • alpha-methyl-acyl-CoA Racemase

Abstract

BACKGROUND

Alpha-methylacyl-CoA racemase (AMACR) is a mitochondrial and peroxisomal enzyme that is overexpressed in prostate cancer. Alternatively spliced variants of AMACR have recently been reported, however, their role in prostate cancer pathogenesis is unclear.

METHODS

Using PCR techniques we have identified a novel variant of AMACR.

RESULTS

This transcript arises by an alternative splicing event in the 5th exon of the gene whereby a 749 base sequence is deleted causing a shift in the reading frame. The protein encoded by this transcript has a predicted molecular weight of 43,833 kDa and a pI of 7.01 and therefore differs in size and physical characteristics from the main form of AMACR. The carboxyl terminus of this variant does not contain the peroxisomal targeting signal found in the main form of AMACR. Using real time PCR it was demonstrated that this transcript also occurs in normal prostate tissue and is elevated in prostate cancer. Coordinate expression of this transcript with the other forms of AMACR was shown. This transcript was expressed as a FLAG fusion protein in Cos-7 cells and probed with relevant antibodies.

CONCLUSION

A deletion event in exon 5 of the AMACR gene creates a novel transcript that is coordinately expressed with the other forms of AMACR but with different biochemical characteristics. © 2005 Wiley-Liss, Inc.

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