Research Article

Loss of mismatch repair activity in simian virus 40 large T antigen–immortalized BPH-1 human prostatic epithelial cell line

  1. Che-Chung Yeh1,
  2. Celeste Lee1,
  3. Mei-Chuan Huang2,
  4. Rajvir Dahiya1,*

Article first published online: 20 JUL 2001

DOI: 10.1002/mc.1049

Issue

Molecular Carcinogenesis

Molecular Carcinogenesis

Volume 31, Issue 3, pages 145–151, July 2001

Additional Information

How to Cite

Yeh, C.-C., Lee, C., Huang, M.-C. and Dahiya, R. (2001), Loss of mismatch repair activity in simian virus 40 large T antigen–immortalized BPH-1 human prostatic epithelial cell line. Mol. Carcinog., 31: 145–151. doi: 10.1002/mc.1049

Author Information

  1. 1

    Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, California

  2. 2

    Department of Pediatrics, University of California, San Francisco, California

*Professor and Director of Urology Research Center (112F), University of California at San Francisco and San Francisco VA Medical Center, 4150 Clement Street, San Francisco, CA 94121.

Publication History

  1. Issue published online: 24 JUL 2001
  2. Article first published online: 20 JUL 2001
  3. Manuscript Accepted: 3 MAY 2001
  4. Manuscript Revised: 5 APR 2001
  5. Manuscript Received: 27 NOV 2000

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Keywords:

  • mismatch repair;
  • SV40 large T antigen;
  • immortalization

Abstract

Simian virus 40 large T antigen (SVLTAg) has been used to immortalize cells; however, the mechanism leading to immortalization is still unclear. We hypothesize that DNA mismatch repair (MMR) activity is important during SVLTAg-induced immortalization. To test this hypothesis, we used the SVLTAg-immortalized cell line BPH-1 derived from human benign prostate epithelial cells to analyze MMR activity and the expression of MMR genes (hMLH1, hPMS1, hPMS2, hMSH2, hMSH3, and hMSH6). The results demonstrated that BPH-1 cells were deficient in repairing G:T, A:C, and G:G mispairs in bacteriophage M13mp2. Reverse-transcription polymerase chain reaction experiments indicated MMR genes (hMSH3, hMSH6, and hPMS1) were expressed at a low level in BPH-1 cells. In contrast, all six MMR genes were expressed in human benign prostate hyperplasia tissues. Downregulation of hMSH3, hMSH6, and hPMS1 genes is not a result of the hypermethylation mechanism because demethylation with 5-aza-2′-deoxycytidine did not restore expression of these genes. Although the hMLH1 gene is expressed in BPH-1 cells, western blotting and exon analyses demonstrated that hMLH1 was mutated and/or deleted in BPH-1 cells. © 2001 Wiley-Liss, Inc.

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