An investigation of Intercellular Adhesion Molecule-1 (ICAM-1) in Breast Cncer
AuthorElston, Bryan George Vincent
Intercellular Adhesion Molecule-1 (ICAM-1, CD54), a cell surface glycoprotein that functions as an integrin, has a well-established role in leukocyte migration during inflammation. Recent studies have indicated a role for this protein in cancer development. In this study three breast cancer cell lines were stimulated with a variety of cytokines. The breast cancer cell lines (MCF7, SK-BR-3 and MDA-MB-468) were chosen to reflect the hormone positive, HER-2 enriched and triple negative subtypes of breast cancer. The cytokines (Interferon gamma, Tumour Necrosis Factor alpha, Interleukin 1beta and Interferon alpha) are commonly encountered in the breast cancer micro-environment. Relative gene expression was measured using quantitative real time polymerase chain reaction. ICAM-1 protein was measured by Western Blot and localised by Immunofluorescence. In addition, ICAM-1 gene expression was measured in human breast cancer samples and ICAM-1 and macrophage (CD68) immunohistochemistry was performed on formalin-fixed, paraffin embedded tumour tissue. ICAM-1 expression was induced in all of the cell lines by IFN, TNF and IL-1 with increased ICAM-1 protein production compared to time-matched controls. IFN appeared to induce ICAM-1 gene expression but no protein was detected. Membranous and para-nuclear ICAM-1 staining was identified after 24 hours in unstimulated MCF7 and MDA-MB-468 cells and the same cell lines stimulated with IFN. ICAM-1 expression was increased in the human tumour tissue compared to normal tissue however this did not correspond with ICAM-1 positivity or numbers of macrophages in the tumour. The study highlights a mechanism that cancer cells may use to enhance their invasive and metastatic potential by making use of a protein normally involved in cell migration.
PublisherUiT Norges arktiske universitet
UiT The Arctic University of Norway
The following license file are associated with this item: