ArticleThe American journal of pathology2001
Loss of heterozygosity on chromosome 11q22-23 in melanoma is associated with retention of the insertion polymorphism in the matrix metalloproteinase-1 promoter.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 47 citations in OpenAlex.
- The BRAF(V600E) inhibitor, PLX4032, increases type I collagen synthesis in melanoma cells.Matrix biology : journal of the International Society for Matrix Biology · 2015Article
- Differential mechanisms of tumor progression in clones from a single heterogeneous human melanoma.Journal of cellular physiology · 2013Article
- Identification of a cigarette smoke-responsive region in the distal MMP-1 promoter.American journal of respiratory cell and molecular biology · 2009Article
- The collagenase-1 (MMP-1) gene promoter polymorphism - 1607/2G is associated with favourable prognosis in patients with colorectal cancer.British journal of cancer · 2007Article
- How matrix metalloproteinases regulate cell behavior.Annual review of cell and developmental biology · 2001Review
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Matrix metalloproteinase-1 (MMP-1, collagenase-1), which degrades interstitial collagen, is expressed at high levels by some tumor cells and is thought to enhance their invasiveness and metastatic potential. We recently described a common single nucleotide insertion polymorphism (2G allele) at -1,607 bp in the promoter of the MMP-1 gene that creates a binding site for the ETS family of transcription factors, and that is associated with enhanced transcription of this gene and increased enzyme activity. Allelic loss at the MMP-1 locus on chromosome 11 occurs in many tumors including melanoma, an invasive and aggressive cancer. We hypothesized that although loss of either the 1G or 2G allele from 1G/2G heterozygotes is random, retention of the transcriptionally more active 2G allele would favor tumor invasion and metastasis. As a result, a higher proportion of metastases would contain the 2G genotype than the 1G genotype. We report here the development of quantitative methods for assessing allelic loss at the MMP-1 locus, and demonstrate that 83% of the metastatic melanomas with loss of heterozygosity at this locus retained the 2G allele. This supports the hypothesis that retention of the 2G allele favors tumor invasion and metastasis in melanoma.
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