ArticleOncotarget2016
Stroma-derived but not tumor ADAMTS1 is a main driver of tumor growth and metastasis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Enhanced expression of ADAMTS1 in ovarian carcinomas: loss of ADAMTS1 expression instigates cellular reprogramming of extracellular matrix ensuing altered plasticity, augmented migration and attenuated adhesion.Journal of biomedical science · 2026Article
- Loss of the extracellular protease ADAMTS1 reveals an antitumorigenic program involving the action of NIDOGEN-1 on macrophage polarization.Oncoimmunology · 2025Article
- Review
- ADAMTS-1 has nuclear localization in cells with epithelial origin and leads to decreased cell migration.Experimental cell research · 2023Article
- Utility of promoter hypermethylation in malignant risk stratification of intraductal papillary mucinous neoplasms.Clinical epigenetics · 2023Article
- ADAMTS proteases and the tumor immune microenvironment: Lessons from substrates and pathologies.Matrix biology plus · 2021Review
- ADAMTS1 Supports Endothelial Plasticity of Glioblastoma Cells with Relevance for Glioma Progression.Biomolecules · 2020Article
- Review
- Article
- Article
- ADAMTS1 protease is required for a balanced immune cell repertoire and tumour inflammatory response.Scientific reports · 2018Article
- Stromal Versican Regulates Tumor Growth by Promoting Angiogenesis.Scientific reports · 2017Article
- Cleavage of Fibulin-2 by the aggrecanases ADAMTS-4 and ADAMTS-5 contributes to the tumorigenic potential of breast cancer cells.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The matrix metalloprotease ADAMTS1 (A Disintegrin And Metalloprotease with ThromboSpondin repeats 1) has been involved in tumorigenesis although its contributions appeared ambiguous. To understand the multifaceted actions of this protease, it is still required a deeper knowledge of its implication in heterogeneous tumor-stroma interactions. Using a syngeneic B16F1 melanoma model in wild type and ADAMTS1 knockout mice we found distinct stroma versus tumor functions for this protease. Genetic deletion of ADAMTS1 in the host microenvironment resulted in a drastic decrease of tumor growth and metastasis. However, the downregulation of tumor ADAMTS1 did not uncover relevant effects. Reduced tumors in ADAMTS1 KO mice displayed a paradoxical increase in vascular density and vascular-related genes; a detailed characterization revealed an impaired vasculature, along with a minor infiltration of macrophages. In addition, ex-vivo assays supported a chief role for ADAMTS1 in vascular sprouting, and melanoma xenografts showed a relevant induction of its expression in stroma compartments. These findings provide the first genetic evidence that supports the pro-tumorigenic role of stromal ADAMTS1.
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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.