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pubmed-article:11485830pubmed:abstractTextThe human myelocytic leukemia cell line HL-60 is a useful model for the study of cellular differentiation. Phorbol 12-myristate 13-acetate (PMA) induces the monocyte/macrophage-like differentiation of HL-60 cells and results in growth arrest, increasing adherence. In PMA-induced differentiation of HL-60 cells, phosphoinositide 3-kinase (PI 3-K) activity was measured as phosphatidylinositol3P recovery from phosphatidylinositol by in vitro kinase assay. PI 3-K activity was increased in HL-60 cells that were stimulated by 20 nM PMA and the activity was inhibited by pretreatment with 20 microM LY294002, a specific inhibitor of PI 3-K. Members of the protein kinase C (PKC) family have been suggested to be one of the downstream targets of PI 3-K. PKC zeta is one of the atypical PKCs, non-diacylglycerol-responsive PKCs, and the activity was measured by the ability of phosphorylation onto myelin basic protein. PMA also induced the activation of PKC zeta during monocytic differentiation of HL-60 cells, and LY294002-pretreated cells failed to induce PKC zeta activation. The activity of PI 3-K is essential for PKC zeta activation, and LY294002 blocks both monocytic differentiation of HL-60 cells and activation of PKC zeta during PMA-induced cell differentiation. This implies that activated PI 3-K subsequently stimulates the PKC zeta in the process of PMA-induced monocytic differentiation.lld:pubmed
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pubmed-article:11485830pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:11485830pubmed:articleTitleThe activation of PI 3-K and PKC zeta in PMA-induced differentiation of HL-60 cells.lld:pubmed
pubmed-article:11485830pubmed:affiliationCollege of Pharmacy and Center of Oriental Medicinal Science, Wonkwang University, Iksan, 570-749, Chonbuk, South Korea.lld:pubmed
pubmed-article:11485830pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11485830pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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