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

研究成果: Article査読

53 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)575-583
ページ数9
ジャーナルCellular Signalling
15
6
DOI
出版ステータスPublished - 2003 6月 1

ASJC Scopus subject areas

  • 細胞生物学

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