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 journalArticle

55 Citations (Scopus)

Abstract

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
Volume57
Issue number2
StatePublished - 1997

Fingerprint

DNA Mismatch Repair
Cell Cycle
S Phase
Messenger RNA
G1 Phase
Genes
Proteins
Hereditary Nonpolyposis Colorectal Neoplasms
cdc Genes
DNA Repair
Fibroblasts
Lung
Mutation
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Meyers, M., Theodosiou, M., Acharya, S., Odegaard, E., Wilson, T., Lewis, J. E., ... Boothman, D. A. (1997). Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2. Cancer Research, 57(2), 206-208.

Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2. / Meyers, Mark; Theodosiou, Maria; Acharya, Samir; Odegaard, Eric; Wilson, Teresa; Lewis, Janet E.; Davis, T. W.; Wilson-Van Patten, Carmell; Fishel, Richard; Boothman, David A.

In: Cancer Research, Vol. 57, No. 2, 1997, p. 206-208.

Research output: Contribution to journalArticle

Meyers, M, Theodosiou, M, Acharya, S, Odegaard, E, Wilson, T, Lewis, JE, Davis, TW, Wilson-Van Patten, C, Fishel, R & Boothman, DA 1997, 'Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2', Cancer Research, vol. 57, no. 2, pp. 206-208.
Meyers M, Theodosiou M, Acharya S, Odegaard E, Wilson T, Lewis JE et al. Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2. Cancer Research. 1997;57(2):206-208.
Meyers, Mark ; Theodosiou, Maria ; Acharya, Samir ; Odegaard, Eric ; Wilson, Teresa ; Lewis, Janet E. ; Davis, T. W. ; Wilson-Van Patten, Carmell ; Fishel, Richard ; Boothman, David A. / Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2. In: Cancer Research. 1997 ; Vol. 57, No. 2. pp. 206-208.
@article{93923491efc64560993a56fb72cfd733,
title = "Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2",
abstract = "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.",
author = "Mark Meyers and Maria Theodosiou and Samir Acharya and Eric Odegaard and Teresa Wilson and Lewis, {Janet E.} and Davis, {T. W.} and {Wilson-Van Patten}, Carmell and Richard Fishel and Boothman, {David A.}",
year = "1997",
language = "English (US)",
volume = "57",
pages = "206--208",
journal = "Journal of Cancer Research",
issn = "0099-7013",
publisher = "American Association for Cancer Research Inc.",
number = "2",

}

TY - JOUR

T1 - Cell cycle regulation of the human DNA mismatch repair genes hMSH2, hMLH1, and hPMS2

AU - Meyers, Mark

AU - Theodosiou, Maria

AU - Acharya, Samir

AU - Odegaard, Eric

AU - Wilson, Teresa

AU - Lewis, Janet E.

AU - Davis, T. W.

AU - Wilson-Van Patten, Carmell

AU - Fishel, Richard

AU - Boothman, David A.

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=15444355644&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=15444355644&partnerID=8YFLogxK

M3 - Article

C2 - 9000555

AN - SCOPUS:15444355644

VL - 57

SP - 206

EP - 208

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0099-7013

IS - 2

ER -