ArticleCancer research2013
Trask loss enhances tumorigenic growth by liberating integrin signaling and growth factor receptor cross-talk in unanchored cells.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Overexpression of a disintegrin and metalloproteinase 9 (ADAM9) in relation to poor prognosis of patients with oral squamous cell carcinoma.Discover oncology · 2024Article
- CDCP1 regulates retinal pigmented epithelial barrier integrity for the development of experimental autoimmune uveitis.JCI insight · 2022Article
- Targeting a proteolytic neoepitope on CUB domain containing protein 1 (CDCP1) for RAS-driven cancers.The Journal of clinical investigation · 2022Article
- CDCP1 on Dendritic Cells Contributes to the Development of a Model of Kawasaki Disease.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- CDCP1 promotes compensatory renal growth by integrating Src and Met signaling.Life science alliance · 2021Article
- Loss of CDCP1 triggers FAK activation in detached prostate cancer cells.American journal of clinical and experimental urology · 2021Article
- An oncogenic viral interferon regulatory factor upregulates CUB domain-containing protein 1 to promote angiogenesis by hijacking transcription factor lymphoid enhancer-binding factor 1 and metastasis suppressor CD82.Cell death and differentiation · 2020Article
- Theranostic Targeting of CUB Domain Containing Protein 1 (CDCP1) in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- CDCP1 overexpression drives prostate cancer progression and can be targeted in vivo.The Journal of clinical investigation · 2020Article
- MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer.British journal of cancer · 2020Article
- Src Kinase Is Biphosphorylated at Y416/Y527 and Activates the CUB-Domain Containing Protein 1/Protein Kinase C δ Pathway in a Subset of Triple-Negative Breast Cancers.The American journal of pathology · 2020Article
- Regulation of inside-out β1-integrin activation by CDCP1.Oncogene · 2018Article
- CD318 is a ligand for CD6.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- CDCP1 drives triple-negative breast cancer metastasis through reduction of lipid-droplet abundance and stimulation of fatty acid oxidation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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- Identification of anti-tumour biologics using primary tumour models, 3-D phenotypic screening and image-based multi-parametric profiling.Molecular cancer · 2015Article
- Significance of Trask protein interactions in brain metastatic cohorts of lung cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
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Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The cell surface glycoprotein Trask/CDCP1 is phosphorylated during anchorage loss in epithelial cells in which it inhibits integrin clustering, outside-in signaling, and cell adhesion. Its role in cancer has been difficult to understand, because of the lack of a discernible pattern in its various alterations in cancer cells. To address this issue, we generated mice lacking Trask function. Mammary tumors driven by the PyMT oncogene and skin tumors driven by the SmoM2 oncogene arose with accelerated kinetics in Trask-deficient mice, establishing a tumor suppressing function for this gene. Mechanistic investigations in mammary tumor cell lines derived from wild-type or Trask-deficient mice revealed a derepression of integrin signaling and an enhancement of integrin-growth factor receptor cross-talk, specifically in unanchored cell states. A similar restrictive link between anchorage and growth in untransformed epithelial cells was observed and disrupted by elimination of Trask. Together our results establish a tumor-suppressing function in Trask that restricts epithelial cell growth to the anchored state.
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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.