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CEACAM1

Official Full Name
CEA cell adhesion molecule 1
Organism
Homo sapiens
GeneID
634
Background
This gene encodes a member of the carcinoembryonic antigen (CEA) gene family, which belongs to the immunoglobulin superfamily. Two subgroups of the CEA family, the CEA cell adhesion molecules and the pregnancy-specific glycoproteins, are located within a 1.2 Mb cluster on the long arm of chromosome 19. Eleven pseudogenes of the CEA cell adhesion molecule subgroup are also found in the cluster. The encoded protein was originally described in bile ducts of liver as biliary glycoprotein. Subsequently, it was found to be a cell-cell adhesion molecule detected on leukocytes, epithelia, and endothelia. The encoded protein mediates cell adhesion via homophilic as well as heterophilic binding to other proteins of the subgroup. Multiple cellular activities have been attributed to the encoded protein, including roles in the differentiation and arrangement of tissue three-dimensional structure, angiogenesis, apoptosis, tumor suppression, metastasis, and the modulation of innate and adaptive immune responses. Multiple transcript variants encoding different isoforms have been reported, but the full-length nature of all variants has not been defined. [provided by RefSeq, May 2010]
Synonyms
BGP; BGP1; BGPI;
Protein Sequence
MGHLSAPLHRVRVPWQGLLLTASLLTFWNPPTTAQLTTESMPFNVAEGKEVLLLVHNLPQQLFGYSWYKGERVDGNRQIVGYAIGTQQATPGPANSGRETIYPNASLLIQNVTQNDTGFYTLQVIKSDLVNEEATGQFHVYPELPKPSISSNNSNPVEDKDAVAFTCEPETQDTTYLWWINNQSLPVSPRLQLSNGNRTLTLLSVTRNDTGPYECEIQNPVSANRSDPVTLNVTYGPDTPTISPSDTYYRPGANLSLSCYAASNPPAQYSWLINGTFQQSTQELFIPNITVNNSGSYTCHANNSVTGCNRTTVKTIIVTELSPVVAKPQIKASKTTVTGDKDSVNLTCSTNDTGISIRWFFKNQSLPSSERMKLSQGNTTLSINPVKREDAGTYWCEVFNPISKNQSDPIMLNVNYNALPQENGLSPGAIAGIVIGVVALVALIAVALACFLHFGKTGRASDQRDLTEHKPSVSNHTQDHSNDPPNKMNEVTYSTLNFEAQQPTQPTSASPSLTATEIIYSEVKKQ
Open
Disease
Solid tumour/cancer
Approved Drug
0
Clinical Trial Drug
2 +
Discontinued Drug
0

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Detailed Information

Found on the long arm of human chromosome 19, the CEACAM1 gene is a member of the carcinoembryonic antigen (CEA) family, which also comprises glycoproteins relevant for pregnancy. Multiple isoforms produced by splicing from the CEACAM1 gene show varying actions on the cell surface. For example, although those with short cytoplasmic tails (S isoforms) have various regulating activities, isoforms with a long cytoplasmic tail (L isoforms) usually play inhibitory roles in immune responses by including immune receptor tyrosine-based inhibitory motifs (ITIM).

Figure 1 illustrates the structure, oligomerization, activation, and targeted intervention of CEACAM1, detailing human and mouse isoform variations, interaction surfaces, and the impact of antibodies on CEACAM1-mediated signaling pathways.Figure 1. CEACAM1 structure, oligomerization, activation, and targeted intervention. (Kim WM, et al., 2019)

Cell Adhesion and Immune Regulation

To control intercellular adhesion, CEACAM1—a calcium-independent cell adhesion molecule—interacts with other cell surface molecules either homophistically or heterophistically. For immune cell interactions, tissue development, angiogenesis, and more, this adherence is very essential. Expressed on T cells, natural killer (NK) cells, and neutrophils among other immune cells, CEACAM1 helps control their immunological activity.

T Cell Regulation: CEACAM1 expression on T cells is intimately correlated with negative immune response control. Using its L isoform, CEACAM1 may suppress TCR-mediated cytotoxic responses, hence halting T cell multiplication and cytokine generation. Maintaining immunological homeostasis, avoiding autoimmune disorders, and stopping tumor immune escape depend on this pathway.

NK Cell Regulation: CEACAM1 also alters NK cell cytotoxic properties. Research indicates that CEACAM1 interactions with molecules on target cells reduce NK cell cytotoxicity. In malignancies devoid of MHC I molecules, including melanoma, CEACAM1 expression is intimately linked to NK cell inhibition.

Neutrophil Activation: Neutrophil activation and death control are functions of CEACAM1. Utilizing the ITIM motif, CEACAM1 may attract SHP-1, thus preventing neutrophilogical responses and inflammatory reactions, thus reducing too strong immunological reactions and tissue damage.

Angiogenesis and Immune Regulation

Beyond its function in immune cells, CEACAM1 is important in angiogenesis and tissue healing. CEACAM1 helps to promote endothelial cell differentiation and migration, therefore facilitating vascular remodeling and angiogenesis—especially in tissue healing after ischemia damage. Crucially for vascular physiological processes, CEACAM1 controls nitric oxide generation via the VEGFR2 signaling pathway and modulates vascular permeability.

Insulin Action and Metabolic Regulation

Insulin action and metabolic control depend on CEACAM1 in significant measure. Research show CEACAM1 may interact with FASN (fatty acid synthase) to control fatty acid production, control insulin signaling pathways, and hasten insulin clearance. Particularly important in hepatic lipogenesis, this ability may have therapeutic effects for metabolic disorders like diabetes.

Tumor Immune Evasion

The immune regulating ability of CEACAM1 makes it a major actor in tumor immune evasion. Immune evasion in different kinds of tumors is linked to too strong expression of CEACAM1. CEACAM1 helps tumor cells avoid host immune surveillance by suppressing T cell and NK cell immunological responses. Potential anti-tumor treatments include immunotherapy approaches aiming at CEACAM1, particularly those aiming at its interaction with immune cells, especially those inhibiting this interaction.

Infection Immune Evasion

Apart from its function in tumor immune evasion, several infections target CEACAM1 as a target to attach to and attack host cells. For example, certain Neisseria bacteria attach to CEACAM1 to help colonization and invasion, therefore improving microbial survival and generating immune suppression to evade host immune clearance.

Autoimmunity and Immune Homeostasis

By suppressing too strong immune responses and hence avoiding autoimmune disorders, CEACAM1 is essential in preserving immunological homeostasis. For T cell responses, for instance, CEACAM1 controls immunological tolerance and stops too strong cytokine replies, and CEACAM1's expression and function may be disturbed in autoimmune illnesses such as rheumatoid arthritis and systemic lupus erythematosus, therefore it might be a target for therapy.

Targeted Therapy and Future Prospects of CEACAM1

Targeted CEACAM1 therapeutics are starting to take the front stage in immunotherapy as CEACAM1 research spans immunoregulation, tumor immune evasion, and infection immune evasion advances. Modern research has looked at employing immune checkpoint inhibitors and monoclonal antibodies to upset CEACAM1 connections with immune cells, hence restoring immunological function against cancer and infections.

Furthermore, considering CEACAM1's function in insulin action and metabolic control, researchers are investigating its possible uses in the treatment of metabolic diseases. CEACAM1 is a multifunctional immunoregulatory molecule with wide therapeutic uses in immunotherapy, metabolic illness treatment, and infection immune evasion.

References:

  1. Kim WM, Huang YH, et al. CEACAM1 structure and function in immunity and its therapeutic implications. Semin Immunol. 2019 Apr;42:101296.
  2. Turcu G, Nedelcu RI, et al. CEACAM1: Expression and Role in Melanocyte Transformation. Dis Markers. 2016;2016:9406319.
  3. Ling Y, Wang J, et al. Roles of CEACAM1 in cell communication and signaling of lung cancer and other diseases. Cancer Metastasis Rev. 2015 Jun;34(2):347-57.
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