Role of liver ICAM-1 in metastasis.

Oncol Lett

Department of Cell Biology and Histology, School of Medicine and Nursing, University of The Basque Country, UPV/EHU, Leioa, E-48940 Vizcaya, Spain.

Published: October 2017

AI Article Synopsis

  • ICAM-1 is a glycoprotein involved in immune response, expressed in various cells such as endothelial cells and leukocytes, and plays a role in physiological processes.
  • ICAM-1 is also found in several cancer types, like melanoma and colorectal cancer, but most research has focused on its expression on tumor cells rather than at metastatic sites.
  • In the liver, ICAM-1 expression is crucial, particularly during inflammation, and understanding its mechanisms could aid in developing new anticancer therapies targeting liver metastasis.

Article Abstract

Intercellular adhesion molecule (ICAM)-1, is a transmembrane glycoprotein of the immunoglobulin (Ig)-like superfamily, consisting of five extracellular Ig-like domains, a transmembrane domain and a short cytoplasmic tail. ICAM-1 is expressed in various cell types, including endothelial cells and leukocytes, and is involved in several physiological processes. Furthermore, it has additionally been reported to be expressed in various cancer cells, including melanoma, colorectal cancer and lymphoma. The majority of studies to date have focused on the expression of the ICAM-1 on the surface of tumor cells, without research into ICAM-1 expression at sites of metastasis. Cancer cells frequently metastasize to the liver, due to its unique physiology and specialized liver sinusoid capillary network. Liver sinusoidal endothelial cells constitutively express ICAM-1, which is upregulated under inflammatory conditions. Furthermore, liver ICAM-1 may be important during the development of liver metastasis. Therefore, it is necessary to improve the understanding of the mechanisms mediated by this adhesion molecule in order to develop host-directed anticancer therapies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5604125PMC
http://dx.doi.org/10.3892/ol.2017.6700DOI Listing

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