ArticleOncogene2006
TIMP-3 deficiency in the host, but not in the tumor, enhances tumor growth and angiogenesis.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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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Who cites it
24 citing papers in PubMed, 52 citations in OpenAlex.
- Disease specific urinary biomarkers in the central nervous system.Scientific reports · 2023Article
- The extracellular microenvironment in immune dysregulation and inflammation in retinal disorders.Frontiers in immunology · 2023Review
- Tissue Inhibitor of Metalloproteases 3 (TIMP-3): In Vivo Analysis Underpins Its Role as a Master Regulator of Ectodomain Shedding.Membranes · 2022Review
- TIMP1 Indicates Poor Prognosis of Renal Cell Carcinoma and Accelerates TumorigenesisFrontiers in genetics · 2022Article
- Sorsby Fundus Dystrophy Mutation in Tissue Inhibitor of Metalloproteinase 3 (TIMP3) promotes Choroidal Neovascularization via a Fibroblast Growth Factor-dependent Mechanism.Scientific reports · 2019Article
- Review
- TIMP-3 as a therapeutic target for cancer.Therapeutic advances in medical oncology · 2019Review
- Signatures of selection and environmental adaptation across the goat genome post-domestication.Genetics, selection, evolution : GSE · 2018Article
- Sphingosine-1-phosphate suppresses chondrosarcoma metastasis by upregulation of tissue inhibitor of metalloproteinase 3 through suppressing miR-101 expression.Molecular oncology · 2017Article
- TIMPs: versatile extracellular regulators in cancer.Nature reviews. Cancer · 2017Review
- Stroma-derived but not tumor ADAMTS1 is a main driver of tumor growth and metastasis.Oncotarget · 2016Article
- Inhibition of microRNA-126 promotes the expression of Spred1 to inhibit angiogenesis in hepatocellular carcinoma after transcatheter arterial chemoembolization: in vivo study.OncoTargets and therapy · 2016Article
- Tissue inhibitor of metalloproteinase-3 (TIMP3) promotes endothelial apoptosis via a caspase-independent mechanism.Apoptosis : an international journal on programmed cell death · 2015Article
- Article
- Loss of the Timp gene family is sufficient for the acquisition of the CAF-like cell state.Nature cell biology · 2014Article
- Article
- Increased neovascularization in mice lacking tissue inhibitor of metalloproteinases-3.Investigative ophthalmology & visual science · 2011Article
- Proteases in cutaneous malignant melanoma: relevance as biomarker and therapeutic target.Cellular and molecular life sciences : CMLS · 2010Review
- Stromal cell-derived CSF-1 blockade prolongs xenograft survival of CSF-1-negative neuroblastoma.International journal of cancer · 2010Article
- Inhibition of tumor growth and induction of apoptosis in prostate cancer cell lines by overexpression of tissue inhibitor of matrix metalloproteinase-3.Cancer gene therapy · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells, stromal cell compartment and the extracellular matrix (ECM) together generate a multifaceted tumor microenvironment. Matrix metalloproteinases and their tissue inhibitors (TIMPs) provide a means for tumor-stromal interaction during tumorigenesis. Among TIMPs, TIMP-3 is uniquely localized to the ECM and is frequently silenced in human cancers. Here, we asked whether the absence of TIMP-3 in the tumor cell or the host affects the process of tumorigenesis. Timp-3(-/-) ES-cell clones were generated and used to develop teratomas in nude mice. Timp-3(-/-) teratomas showed similar tumor take, growth, and angiogenesis compared to timp-3(+/+) teratomas. To study the effect of TIMP-3 ablation in the host stroma, we measured the growth kinetics of subcutaneous B16F10 melanomas in timp-3(-/-) and wild-type littermates. Tumors grew significantly faster in timp-3(-/-) than in wild-type mice and their CD31 content was significantly higher indicating increased angiogenesis. Augmented angiogenesis in timp-3(-/-) mice was directly tested using Matrigel plug and Gelfoam assays. In response to FGF-2, timp-3(-/-) endothelial cells invaded more efficiently, leading to enhanced formation of functional blood vessels. Thus, TIMP-3 deficiency in the host, but not in the tumor per se, leads to enhanced tumor growth and angiogenesis. TIMP-3 located within the tumor microenvironment inhibits tumorigenesis.
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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.