ArticleOncogene2000
Demonstration in vivo that stromelysin-3 functions through its proteolytic activity.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 76 citations in OpenAlex.
- AnGenes · 2026Article
- The fat and the bad: Mature adipocytes, key actors in tumor progression and resistance.Oncotarget · 2017Review
- CXCR6 expression in non-small cell lung carcinoma supports metastatic process via modulating metalloproteinases.Oncotarget · 2015Article
- Hematopoietic stem cell-derived adipocytes and fibroblasts in the tumor microenvironment.World journal of stem cells · 2015Review
- Functional relationship between matrix metalloproteinase-11 and matrix metalloproteinase-14.Cancer medicine · 2014Article
- Matrix metalloproteinase induction of Rac1b, a key effector of lung cancer progression.Science translational medicine · 2012Article
- Article
- Collagenase-3 expression by tumor cells and gelatinase B expression by stromal fibroblast-like cells are associated with biochemical recurrence after radical prostatectomy in patients with prostate cancer.World journal of urology · 2011Article
- Physiology and pathophysiology of matrix metalloproteases.Amino acids · 2011Review
- Comparative study of stromal metalloproteases expression in patients with benign hyperplasia and prostate cancer.Journal of cancer research and clinical oncology · 2011Article
- Epithelial-mesenchymal Transition and Cell Invasion.Toxicological research · 2010Review
- Matrix metalloproteinase-11/stromelysin-3 exhibits collagenolytic function against collagen VI under normal and malignant conditions.Oncogene · 2008Article
- Matrix metalloproteinases stimulate epithelial-mesenchymal transition during tumor development.Clinical & experimental metastasis · 2008Review
- Regulation of extracellular matrix remodeling and cell fate determination by matrix metalloproteinase stromelysin-3 during thyroid hormone-dependent post-embryonic development.Pharmacology & therapeutics · 2007Review
- Stromelysin-3 over-expression enhances tumourigenesis in MCF-7 and MDA-MB-231 breast cancer cell lines: involvement of the IGF-1 signalling pathway.BMC cancer · 2007Article
- Breast cancer progression: insights into multifaceted matrix metalloproteinases.Clinical & experimental metastasis · 2007Review
- Overexpression of cathepsin F, matrix metalloproteinases 11 and 12 in cervical cancer.BMC cancer · 2005Article
- Membrane associated proteases and their inhibitors in tumour angiogenesis.Journal of clinical pathology · 2004Review
- Specific expression of matrix metalloproteinases 1, 3, 9 and 13 associated with invasiveness of breast cancer cells in vitro.Clinical & experimental metastasis · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stromelysin-3 (ST3), a matrix metalloproteinase (MMP) expressed in aggressive carcinomas, has been shown to promote tumor development in different in vivo experimental models. However, the inability of its mature form to degrade extracellular matrix components casts doubt on whether ST3 functions in vivo as a protease. In this study, we evaluated whether the ST3 tumor-promoting effect could be ascribed to its proteolytic activity and whether this putative protease could be targeted with MMP inhibitors. Catalytically inactive mutant cDNA of human (h) ST3 or mouse (m) ST3 were generated and transfected into MCF7 cells. When injected into nude mice in the presence of matrigel, the mutant-bearing cells did not exhibit the enhanced tumorigenicity elicited by MCF7 cells transfected with wild-type ST3 cDNA. In a second approach, TIMP2 overproduction in MCF7 cells expressing hST3 was induced by retroviral infection. The co-expression of ST3 and TIMP2 failed to enhance the tumorigenicity of MCF7 cells. Notably, matrigel depleted of low-molecular-weight proteins and growth factors failed to promote the tumorigenicity of ST3-expressing MCF7 cells. These findings provide the first in vivo evidence that ST3 is indeed a protease that can modulate cancer progression by remodeling extracellular matrix and probably by inducing it to release the necessary microenvironmental factors. Thus, ST3 represents an interesting target for specific MMP inhibition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.