ArticleOncogene1999
cis-Determinants in the cytoplasmic domain of CEACAM1 responsible for its tumor inhibitory function.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 85 citations in OpenAlex.
- Dual-recognizing antibodies targeting CEACAMs in the tumor microenvironment: towards more precise targeting.Cell communication and signaling : CCS · 2026Review
- Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024Review
- Mechanism and function of CEACAM1 splice isoforms.European journal of clinical investigation · 2024Review
- Proinflammatory and Cancer-Promoting PathobiontBiomolecules · 2022Article
- Roles and mechanisms of circulating CEACAM1 in the cirrhosis-related intestinal hyperpermeability: in vitro approach.Journal of the Chinese Medical Association : JCMA · 2021Article
- The old CEACAMs find their new role in tumor immunotherapy.Investigational new drugs · 2020Review
- CEACAM1 in Liver Injury, Metabolic and Immune Regulation.International journal of molecular sciences · 2018Review
- Article
- Prognostic Impact of CEACAM1 in Node-Negative Ovarian Cancer Patients.Disease markers · 2018Article
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- Negative immune checkpoints on T lymphocytes and their relevance to cancer immunotherapy.Molecular oncology · 2015Review
- High-fat diet amplifies renal renin angiotensin system expression, blood pressure elevation, and renal dysfunction caused by Ceacam1 null deletion.American journal of physiology. Endocrinology and metabolism · 2015Article
- CEACAM1 promotes melanoma cell growth through Sox-2.Neoplasia (New York, N.Y.) · 2014Article
- Inside-out signaling promotes dynamic changes in the carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1) oligomeric state to control its cell adhesion properties.The Journal of biological chemistry · 2013Article
- CEACAM1 on activated NK cells inhibits NKG2D-mediated cytolytic function and signaling.European journal of immunology · 2013Article
- The transmembrane domain of CEACAM1-4S is a determinant of anchorage independent growth and tumorigenicity.PloS one · 2012Article
- Genetic alterations and expression pattern of CEACAM1 in colorectal adenomas and cancers.Pathology oncology research : POR · 2011Article
- Generation of human CEACAM1 transgenic mice and binding of Neisseria Opa protein to their neutrophils.PloS one · 2010Article
- Systemic dysregulation of CEACAM1 in melanoma patients.Cancer immunology, immunotherapy : CII · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CEACAM1, also known as C-CAM, BGP and CD66a, is a member of the carcinoembryonic antigen (CEA) family which is itself part of the immunoglobulin supergene family. CEACAM1 is involved in intercellular adhesion, signal transduction and tumor cell growth regulation. CEACAM1 is down-regulated in colon and prostate carcinomas, as well as in endometrial, bladder and hepatic tumors, and 30% of breast cancers. We have shown in a mouse colon tumor model that CEACAM1 with a long cytoplasmic domain inhibited the development of tumors whereas a splice variant lacking the cytoplasmic domain did not. In this study, we define the subregions of the long cytoplasmic domain participating in the tumor inhibition phenotype of CEACAM1. We show that a single point mutation of Tyr488, conforming to an Immunoreceptor Tyrosine Inhibition Motif (ITIM), was sufficient to reverse the in vivo tumor cell growth inhibition. Substitution or deletion of residues in the C-terminal region of the CEACAM1 cytoplasmic domain also led to reversal of tumor cell growth inhibition. This result is in agreement with our previous studies demonstrating the C-terminal region of the cytoplasmic domain influences the levels of CEACAM1 Tyr phosphorylation and its association with the protein Tyr phosphatases SHP-1 and SHP-2. Furthermore, removal of the N-terminal domain of CEACAM1, essential for intercellular adhesion, did not impair the tumor inhibitory effect. These results suggest that Tyr phosphorylation or dephosphorylation of the CEACAM1 cytoplasmic domain represents a crucial step in the control of epithelial cell proliferation.
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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.