ArticleInternational journal of cancer2008
Breast cancer-associated mutations in metalloprotease disintegrin ADAM12 interfere with the intracellular trafficking and processing of the protein.
Article in International journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- ADAM12 abrogation alters immune cell infiltration and improves response to checkpoint blockade therapy in the T11 murine model of triple-negative breast cancer.Oncoimmunology · 2023Article
- Mutational drivers of cancer cell migration and invasion.British journal of cancer · 2021Review
- Article
- Pericellular proteolysis in cancer.Genes & development · 2014Review
- Phenotypic diversity of breast cancer-related mutations in metalloproteinase-disintegrin ADAM12.PloS one · 2014Article
- Molecular profiling of ADAM12 and ADAM17 genes in human malignant melanoma.Pathology oncology research : POR · 2013Article
- Metalloproteinase-disintegrin ADAM12 is associated with a breast tumor-initiating cell phenotype.Breast cancer research and treatment · 2013Article
- Article
- An essential role of metalloprotease-disintegrin ADAM12 in triple-negative breast cancer.Breast cancer research and treatment · 2012Article
- Somatic mutations in the Notch, NF-KB, PIK3CA, and Hedgehog pathways in human breast cancers.Genes, chromosomes & cancer · 2012Article
- Functional analysis of a breast cancer-associated mutation in the intracellular domain of the metalloprotease ADAM12.PloS one · 2012Article
- Structural and functional impact of cancer-related missense somatic mutations.Journal of molecular biology · 2011Article
- Metalloprotease-disintegrin ADAM12 expression is regulated by Notch signaling via microRNA-29.The Journal of biological chemistry · 2011Article
- ADAM12 and ADAM17 gene expression in laser-capture microdissected and non-microdissected breast tumors.Pathology oncology research : POR · 2011Article
- The role of SnoN in transforming growth factor beta1-induced expression of metalloprotease-disintegrin ADAM12.The Journal of biological chemistry · 2010Article
- Metal-proteinase ADAM12, kinesin 14 and checkpoint suppressor 1 as new molecular markers of laryngeal carcinoma.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2009Article
- Differential gene expression analysis of subcutaneous fat, fascia, and skin overlying a Dupuytren's disease nodule in comparison to control tissue.Hand (New York, N.Y.) · 2009Article
- The role of Delta-like 1 shedding in muscle cell self-renewal and differentiation.Journal of cell science · 2008Article
- RACK1, a new ADAM12 interacting protein. Contribution to liver fibrogenesis.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
ADAM12 has recently emerged as a Candidate Cancer Gene in a comprehensive genetic analysis of human breast cancers. Three somatic mutations in ADAM12 were observed at significant frequencies in breast cancers: D301H, G479E and L792F. The first 2 of these mutations involve highly conserved residues in ADAM12, and our computational sequence analysis confirms that they may be cancer-related. We show that the corresponding mutations in mouse ADAM12 inhibit the proteolytic processing and activation of ADAM12 in NIH3T3, COS-7, CHO-K1 cells and in MCF-7 breast cancer cells. The D/H and G/E ADAM12 mutants exert a dominant-negative effect on the processing of the wild-type ADAM12. Immunofluorescence analysis and cell surface biotinylation experiments demonstrate that the D/H and G/E mutants are retained inside the cell and are not transported to the cell surface. Consequently, the D/H and G/E mutants, unlike the wild-type ADAM12, are not capable of shedding Delta-like l, a ligand for Notch receptor, at the cell surface, or of stimulating cell migration. Our results suggest that the breast cancer-associated mutations interfere with the intracellular trafficking of ADAM12 and result in loss of the functional ADAM12 at the cell surface.
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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.