ArticlePloS one2016
ADAM15 Is Functionally Associated with the Metastatic Progression of Human Bladder Cancer.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Loss of ADAM15 prevents necroptosis induction by partial RIPK1 degradation due to enhanced TNF-R1 surface expression and basal caspase-8 activation.Cell communication and signaling : CCS · 2025Article
- The emerging role of human transmembrane RGD-based counter-receptors of integrins in health and disease.Cellular & molecular biology letters · 2025Review
- A Disintegrin and Metalloprotease 15 (ADAM15) as a Potential Predictor of Distant Metastasis in Colorectal Cancer (CRC).Journal of clinical medicine · 2025Article
- Characterization of circulating tumor cells in patients with metastatic bladder cancer utilizing functionalized microfluidics.Neoplasia (New York, N.Y.) · 2024Article
- Association of ADAM family members with proliferation signaling and disease progression in multiple myeloma.Blood cancer journal · 2024Article
- Article
- Clinicopathological and prognostic significance of Ephrin A3 in bladder urothelial carcinoma.Oncology letters · 2023Article
- Glioma Cells Expressing High Levels of ALDH5A1 Exhibit Enhanced Migration Transcriptional Signature in Patient Tumors.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Integrin α3/α6 and αV are implicated in ADAM15-activated FAK and EGFR signalling pathway individually and promote non-small-cell lung cancer progression.Cell death & disease · 2022Article
- ADAM15 correlates with prognosis, immune infiltration and apoptosis in hepatocellular carcinoma.Aging · 2021Article
- N-cadherin in osteolineage cells modulates stromal support of tumor growth.Journal of bone oncology · 2021Article
- Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage.Osteoarthritis and cartilage open · 2020Article
- The microRNA miR-3174 Suppresses the Expression of ADAM15 and Inhibits the Proliferation of Patient-Derived Bladder Cancer Cells.OncoTargets and therapy · 2020Article
- ADAM proteases: Emerging role and targeting of the non-catalytic domains.Cancer letters · 2019Review
- ADAM15 mediates upregulation of Claudin-1 expression in breast cancer cells.Scientific reports · 2019Article
- Novel cooperative pathway of c-Myc and Furin, a pro-protein convertase, in cell proliferation as a therapeutic target in ovarian cancers.Oncotarget · 2018Article
- Article
- Actein induces autophagy and apoptosis in human bladder cancer by potentiating ROS/JNK and inhibiting AKT pathways.Oncotarget · 2017Article
- Exploiting poly(I:C) to induce cancer cell apoptosis.Cancer biology & therapy · 2017Review
- LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
ADAM15 is a member of a family of catalytically active disintegrin membrane metalloproteinases that function as molecular signaling switches, shed membrane bound growth factors and/or cleave and inactivate cell adhesion molecules. Aberrant metalloproteinase function of ADAM15 may contribute to tumor progression through the release of growth factors or disruption of cell adhesion. In this study, we utilized human bladder cancer tissues and cell lines to evaluate the expression and function of ADAM15 in the progression of human bladder cancer. Examination of genome and transcriptome databases revealed that ADAM15 ranked in the top 5% of amplified genes and its mRNA was significantly overexpressed in invasive and metastatic bladder cancer compared to noninvasive disease. Immunostaining of a bladder tumor tissue array designed to evaluate disease progression revealed increased ADAM15 immunoreactivity associated with increasing cancer stage and exhibited significantly stronger staining in metastatic samples. About half of the invasive tumors and the majority of the metastatic cases exhibited high ADAM15 staining index, while all low grade and noninvasive cases exhibited negative or low staining. The knockdown of ADAM15 mRNA expression significantly inhibited bladder tumor cell migration and reduced the invasive capacity of bladder tumor cells through MatrigelTM and monolayers of vascular endothelium. The knockdown of ADAM15 in a human xenograft model of bladder cancer inhibited tumor growth by 45% compared to controls. Structural modeling of the catalytic domain led to the design of a novel ADAM15-specific sulfonamide inhibitor that demonstrated bioactivity and significantly reduced the viability of bladder cancer cells in vitro and in human bladder cancer xenografts. Taken together, the results revealed an undescribed role of ADAM15 in the invasion of human bladder cancer and suggested that the ADAM15 catalytic domain may represent a viable therapeutic target in patients with advanced disease.
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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.