Prohibition gene is overexpressed but not mutated in rat bladder carcinomas and cell lines

Makoto Asamoto, Samuel Monroe Cohen

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

Prohibitin was isolated as a candidate antiproliferating gene in rat liver cells, and it has been suggested as a tumor suppressor gene in human breast cancer. We investigated the steady state level of prohibitin mRNA in rat bladder cell lines and in rat bladder carcinoma induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) and sodium saccharin, as well as the protein level in rat bladder epithelial cells. We also examined the prohibitin gene for mutations using the polymerase chain reaction (PCR) single strand conformation polymorphism (SSCP) and direct sequencing methods. All rat bladder tumors investigated and several cell lines had unexpectedly increased steady state levels of prohibitin mRNA compared with that of normal rat bladder or liver. The prohibitin protein was easily detected by Western blotting in all cell lines regardless of their malignant status or growth rate. However, PCR-SSCP and direct sequencing analysis showed no mutations in the prohibitin gene. These results indicate that prohibitin overexpression, but not mutations, may be involved in the early stage of rat bladder carcinogenesis.

Original languageEnglish (US)
Pages (from-to)201-207
Number of pages7
JournalCancer Letters
Volume83
Issue number1-2
DOIs
Publication statusPublished - Aug 15 1994

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Keywords

  • Bladder carcinoma
  • FANFT
  • Prohibitin
  • Rat
  • Saccharin

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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