ArticleBreast cancer research and treatment2013
Metalloproteinase-disintegrin ADAM12 is associated with a breast tumor-initiating cell phenotype.
Article in Breast cancer research and treatment, 2013. 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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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, 25 citations in OpenAlex.
- A disintegrin and metallopeptidase domain (ADAM) 12, ADAM 17 mRNA and ADAM10 protein hold potential as biomarkers for detection of early gastric cancer.Scientific reports · 2025Article
- A disintegrin and metalloprotease 12 contributes to colorectal cancer metastasis by regulating epithelial‑mesenchymal transition.International journal of oncology · 2023Article
- 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
- Hypoxia-inducible factor-dependent ADAM12 expression mediates breast cancer invasion and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells.International journal of oncology · 2020Article
- ADAM12 is A Potential Therapeutic Target Regulated by Hypomethylation in Triple-Negative Breast Cancer.International journal of molecular sciences · 2020Article
- Proteomic screening identifies the zonula occludens protein ZO-1 as a new partner for ADAM12 in invadopodia-like structures.Oncotarget · 2018Article
- ADAM12 Is a Novel Regulator of Tumor Angiogenesis via STAT3 Signaling.Molecular cancer research : MCR · 2017Article
- Metalloprotease-dependent activation of EGFR modulates CD44Breast cancer research and treatment · 2017Article
- ADAM12-L confers acquired 5-fluorouracil resistance in breast cancer cells.Scientific reports · 2017Article
- Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer.Molecular cancer · 2017Article
- The ADAMs family of proteases as targets for the treatment of cancer.Cancer biology & therapy · 2016Review
- Protein disulfide isomerases in the endoplasmic reticulum promote anchorage-independent growth of breast cancer cells.Breast cancer research and treatment · 2016Article
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- ADAM12 is a prognostic factor associated with an aggressive molecular subtype of high-grade serous ovarian carcinoma.Carcinogenesis · 2015Article
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- The Disintegrin and Metalloprotease ADAM12 Is Associated with TGF-β-Induced Epithelial to Mesenchymal Transition.PloS one · 2015Article
- Phenotypic diversity of breast cancer-related mutations in metalloproteinase-disintegrin ADAM12.PloS one · 2014Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Members of the ADAM family of proteases have been associated with mammary tumorigenesis. Gene profiling of human breast tumors identified several intrinsic subtypes of breast cancer, which differ in terms of their basic biology, response to chemotherapy/radiation, preferential sites of metastasis, and overall patient survival. Whether or not the expression of individual ADAM proteases is linked to a particular subtype of breast cancer and whether the functions of these ADAMs are relevant to the cancer subtype have not been investigated. We analyzed several transcriptomic datasets and found that ADAM12L is specifically up-regulated in claudin-low tumors. These tumors are poorly differentiated, exhibit aggressive characteristics, have molecular signatures of epithelial-to-mesenchymal transition (EMT), and are rich in markers of breast tumor-initiating cells (BTICs). Consistently, we find that ADAM12L, but not the alternative splice variant ADAM12S, is a part of stromal, mammosphere, and EMT gene signatures, which are all associated with BTICs. In patients with estrogen receptor-negative tumors, high expression of ADAM12L, but not ADAM12S, is predictive of resistance to neoadjuvant chemotherapy. Using MCF10DCIS.com breast cancer cells, which express the endogenous ADAM12L and efficiently form mammospheres when plated at the density of single cell per well, we show that ADAM12L plays an important role in supporting mammosphere growth. We postulate that ADAM12L may serve as a novel marker and/or a novel therapeutic target in BTICs.
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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.