FAK overexpression upregulates cyclin D3 and enhances cell proliferation via the PKC and PI3-kinase-Akt pathways
Autor: | Megumi Funakoshi-Tago, Tadashi Kasahara, Yoshiko Sonoda, Maki Hasegawa, Eriko Aizu-Yokota, Daisuke Yamamoto |
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Rok vydání: | 2003 |
Předmět: |
HL-60 Cells
Protein Serine-Threonine Kinases Transfection Models Biological Retinoblastoma Protein Phosphatidylinositol 3-Kinases Cyclin-dependent kinase Cyclins Proto-Oncogene Proteins Humans Cyclin D3 Protein kinase B Protein Kinase C Protein kinase C Cyclin PTK2B biology Phospholipase C gamma Cell growth Chemistry Cell Cycle Cell Biology Protein-Tyrosine Kinases Cell cycle Cyclin-Dependent Kinases Up-Regulation Cell biology Isoenzymes Focal Adhesion Kinase 1 Focal Adhesion Protein-Tyrosine Kinases Type C Phospholipases Cancer research biology.protein biological phenomena cell phenomena and immunity Proto-Oncogene Proteins c-akt Cell Division Signal Transduction |
Zdroj: | Cellular Signalling. 15:575-583 |
ISSN: | 0898-6568 |
DOI: | 10.1016/s0898-6568(02)00142-0 |
Popis: | We previously demonstrated that FAK-transfected HL-60 (HL-60/FAK) cells exhibit anti-apoptotic capacity. Here, we report that HL-60/FAK cells proliferate much faster than vector-transfected control (HL-60/Vect) cells with a 1.5-fold faster doubling time. This observation prompted us to investigate the mechanism of how HL-60/FAK cells augment cell proliferation. Since a protein kinase C (PKC) inhibitor, chelerythrine, or a PI3-kinase inhibitor, LY294002, suppressed cell proliferation effectively, both PKC and PI-3-kinase pathways are presumed to be involved in the cell proliferation. Among cyclins and CDKs, cyclin D3 expression was particularly prominent in the HL-60/FAK cells. Among PKC family, particularly PKCalpha, beta and eta isoforms were activated and directly associated with FAK in HL-60/FAK cells. We assumed that FAK activates PKC and PI3-kinase-Akt pathway, which resulted in marked induction of cyclin D3 expression and CDK activity. |
Databáze: | OpenAIRE |
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