ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway.

Abstract	ICAM-3 interacts with LFA1, and is involved in the intercellular adhesion of leukocytes as well as in the mainenance of cell survival. It has also been suggested to induce cancer cell proliferation but the precise signaling pathway is unclear. The aim of this study was to determine the ICAM-3-activated downstream pathway in H1299 lung cancer cells. The level of ICAM-3-induced cell growth was examined using BrdU incorporation, which is a colony-forming assay, FACS analysis, and cell counting. The results showed that ICAM-3 expression induces cancer cell proliferation. In addition, FAK, Akt, PDK1, GSK-3beta, BAD, and PTEN were phosphorylated by ICAM-3-overexpression, resulting in enhanced cell proliferation. In conclusion, ICAM-3 expression induces cancer cell proliferation, and an increase in ICAM-3 expression can contribute to cancer progression.
Authors	Yong Geon Kim, Mi Jin Kim, Jong-Seok Lim, Myeong-Sok Lee, Jun Suk Kim, Young Do Yoo
Journal	Cancer letters (Cancer Lett) Vol. 239 Issue 1 Pg. 103-10 (Jul 28 2006) ISSN: 0304-3835 [Print] Ireland
PMID	16137825 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Antigens, CD Cell Adhesion Molecules ICAM3 protein, human Phosphatidylinositol 3-Kinases GSK3B protein, human Glycogen Synthase Kinase 3 beta Proto-Oncogene Proteins c-akt Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Glycogen Synthase Kinase 3 Mitogen-Activated Protein Kinase Kinases PTEN Phosphohydrolase PTEN protein, human
Topics	Antigens, CD (pharmacology) Apoptosis Cell Adhesion Molecules (pharmacology) Cell Cycle Cell Proliferation (drug effects) Colony-Forming Units Assay Glycogen Synthase Kinase 3 (metabolism) Glycogen Synthase Kinase 3 beta Humans Lung Neoplasms (metabolism) Mitogen-Activated Protein Kinase 1 (metabolism) Mitogen-Activated Protein Kinase 3 (metabolism) Mitogen-Activated Protein Kinase Kinases (metabolism) PTEN Phosphohydrolase (metabolism) Phosphatidylinositol 3-Kinases (metabolism) Phosphorylation (drug effects) Proto-Oncogene Proteins c-akt (metabolism) Signal Transduction Tumor Cells, Cultured

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