Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2

Mark Meyers, Maria Theodosiou, Samir Acharya, Eric Odegaard, Teresa Wilson, Janet E. Lewis, T. W. Davis, Carmell Wilson-Van Patten, Richard Fishel, David A. Boothman

Research output: Contribution to journalArticlepeer-review

58 Scopus citations


Hereditary nonpolyposis colorectal cancer is a cancer susceptibility syndrome that has been found to be caused by mutations in any of several genes involved in DNA mismatch repair, including hMSH2, hMLH1, or hPMS2. Recent reports have suggested that hMSH2 and hMLH1 have a rule in the regulation of the cell cycle. To determine if these genes are cell cycle regulated, we examined their mRNA and protein levels throughout the cell cycle in IMR-90 normal human lung fibroblasts. We demonstrate that the levels of hMSH2 mRNA and protein do not change appreciably throughout the cell cycle. Although hMLH1 mRNA levels remained constant, there was a modest (approximately 50%) increase in its protein levels during late G1 and S phase. The levels of hPMS2 mRNA fluctuated (decreasing 50% in G1 and increasing 50% in S phase), whereas hPMS2 protein levels increased 50% in late G1 and S phase. Our data indicate that, at least in normal cells, the machinery responsible for the detection and repair of mismatched DNA bases is present throughout the cell cycle.

Original languageEnglish (US)
Pages (from-to)206-208
Number of pages3
JournalCancer research
Issue number2
StatePublished - 1997

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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