FAK overexpression upregulates cyclin D3 and enhances cell proliferation via the PKC and PI3-kinase-Akt pathways

Daisuke Yamamoto, Yoshiko Sonoda, Maki Hasegawa, Megumi Funakoshi-Tago, Eriko Aizu-Yokota, Tadashi Kasahara

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

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 PKCα, β and η 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.

Original languageEnglish
Pages (from-to)575-583
Number of pages9
JournalCellular Signalling
Volume15
Issue number6
DOIs
Publication statusPublished - 2003 Jun 1

Keywords

  • Akt
  • Cell proliferation
  • Cyclin D3
  • Focal adhesion kinase
  • PKC
  • Phosphatidylinositol 3-kinase

ASJC Scopus subject areas

  • Cell Biology

Fingerprint Dive into the research topics of 'FAK overexpression upregulates cyclin D3 and enhances cell proliferation via the PKC and PI3-kinase-Akt pathways'. Together they form a unique fingerprint.

  • Cite this