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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / pharmacology*
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Apoptosis*
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Cell Adhesion Molecules / pharmacology*
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Cell Cycle
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Cell Proliferation / drug effects*
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Colony-Forming Units Assay
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Glycogen Synthase Kinase 3 / metabolism
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Glycogen Synthase Kinase 3 beta
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Humans
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Lung Neoplasms / metabolism*
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Mitogen-Activated Protein Kinase 1 / metabolism
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Mitogen-Activated Protein Kinase 3 / metabolism
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Mitogen-Activated Protein Kinase Kinases / metabolism
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PTEN Phosphohydrolase / metabolism
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Phosphatidylinositol 3-Kinases / metabolism*
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Phosphorylation / drug effects
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Proto-Oncogene Proteins c-akt / metabolism*
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Signal Transduction
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Tumor Cells, Cultured
Substances
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Antigens, CD
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Cell Adhesion Molecules
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ICAM3 protein, human
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Phosphatidylinositol 3-Kinases
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GSK3B protein, human
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Glycogen Synthase Kinase 3 beta
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Proto-Oncogene Proteins c-akt
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Glycogen Synthase Kinase 3
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Mitogen-Activated Protein Kinase Kinases
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PTEN Phosphohydrolase
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PTEN protein, human