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 language | English (US) |
|---|---|
| Pages (from-to) | 206-208 |
| Number of pages | 3 |
| Journal | Cancer Research |
| Volume | 57 |
| Issue number | 2 |
| State | Published - 1997 |
Fingerprint
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
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 journal › Article
}
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 -