ArticleBritish journal of cancer1999
'Proteolytic switching': opposite patterns of regulation of gelatinase B and its inhibitor TIMP-1 during human melanoma progression and consequences of gelatinase B overexpression.
Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 64 citations in OpenAlex.
- An innovative cellular medicine approach via the utilization of novel nanotechnology-based biomechatronic platforms as a label-free biomarker for early melanoma diagnosis.Scientific reports · 2024Article
- Article
- Neutralization of matrix metalloproteinase-9 potentially enhances oncolytic efficacy of tanapox virus for melanoma therapy.Medical oncology (Northwood, London, England) · 2017Article
- The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Cell reports · 2016Article
- Regulation of TIMP-1 in Human Placenta and Fetal Membranes by lipopolysaccharide and demethylating agent 5-aza-2'-deoxycytidine.Reproductive biology and endocrinology : RB&E · 2015Article
- Epigenetic regulation of mmp-9 gene expression.Cellular and molecular life sciences : CMLS · 2013Review
- Expression of MMP-1, MMP-9 and TIMP-2 in prostate carcinoma and their influence on prognosis and survival.Journal of cancer research and clinical oncology · 2013Article
- Biological stimuli and biomolecules in the assembly and manipulation of nanoscale polymeric particles.Chemical science · 2012Article
- Controlling and switching the morphology of micellar nanoparticles with enzymes.Journal of the American Chemical Society · 2011Article
- Membrane-type-3 matrix metalloproteinase (MT3-MMP) functions as a matrix composition-dependent effector of melanoma cell invasion.PloS one · 2011Article
- Elastin-derived peptides enhance melanoma growth in vivo by upregulating the activation of Mcol-A (MMP-1) collagenase.British journal of cancer · 2010Article
- Protease-activated receptor-1 (PAR-1) promotes the motility of human melanomas and is associated to their metastatic phenotype.Clinical & experimental metastasis · 2010Article
- Tissue inhibitor of metalloproteinase 1 expression associated with gene demethylation confers anoikis resistance in early phases of melanocyte malignant transformation.Translational oncology · 2009Article
- Upregulation of galectin-7 in murine lymphoma cells is associated with progression toward an aggressive phenotype.Leukemia · 2003Article
- Matrix metalloproteinase 9 promoter activity is induced coincident with invasion during tumor progression.The American journal of pathology · 2000Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Although it is generally accepted that proteolytic degradation is an important mechanism used by malignant cells in the process of metastasis, comparatively little is known about the regulation of molecules responsible for proteolysis and how they become de-regulated during human tumour progression. Using a genetically related pair of human melanoma cell lines, derived from the same patient at different stages of disease, we analysed differences in the cytokine-mediated regulation of gelatinase B (MMP-9), an enzyme thought to play an important role in cellular invasiveness, and TIMP-1, a physiological inhibitor of this enzyme. Whereas the advanced stage (i.e. metastatic) partner of this pair (WM 239) could produce gelatinase B upon induction with interleukin (IL)-1beta or tumour necrosis factor alpha (TNF-alpha), the early stage (i.e. primary) partner (WM 115) could not. In sharp contrast, we found that TIMP-1 displayed an opposite pattern of induction in these cell lines. Specifically, the early stage cell line, WM 115, demonstrated a marked increase in the production of TIMP-1 when treated with IL-1beta or TNF-alpha whereas the advanced cell line, WM 239, showed no such increase. Treatment with the DNA demethylating agent, 2-deoxy-5-azacytidine, resulted in a marked up-regulation of both gelatinase B and TIMP-1 in both cell lines. It was further found that constitutive overexpression of gelatinase B in WM 239 cells and an additional melanoma cell line (MeWo), derived from a metastatic lesion, was able to greatly enhance lung colonization in an experimental metastasis assay while we did not observe differences in tumorigenicity. From these results we conclude that an altered responsiveness of gelatinase B and TIMP-1 to induction by similar agents is associated with disease progression in human melanoma and that this altered responsiveness can have consequences to the aggressive nature of the disease.
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Registered trials
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