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Translocation and activation of protein kinase C by the plasma cell tumor-promoting alkane pristane. Cancer Res 1995 Feb 01;55(3):518-24

Date

02/01/1995

Pubmed ID

7834620

Scopus ID

2-s2.0-0028959209 (requires institutional sign-in at Scopus site)   12 Citations

Abstract

Pristane (2,6,10,14-tetramethylpentadecane) is a C19-isoalkane that promotes the development of plasmacytomas in genetically susceptible BALB/c mice. Similarities between the effects of pristane and protein kinase C (PKC)-activating phorbol esters suggested that the tumor promoting activity of pristane might involve the activation of PKC. Here we show that up to 5 mol% of pristane can be homogeneously incorporated into phosphatidylcholine/phosphatidylserine bilayers. Membrane-incorporated pristane partially activated PKC and increased phorbol ester binding to the bilayer by more than 50%. Pristane (50 microM) delivered as an inclusion complex with beta-cyclodextrin to promyelocytic HL-60 leukemia cells induced a partial long-term translocation of PKC to the cell membrane. This was accompanied by differentiation of HL-60 cells into macrophage-like cells. It is concluded that activation of PKC may comprise an important aspect of the tumor promoting potential of pristane.

Author List

Janz S, Gawrisch K, Lester DS

Author

Siegfried Janz MD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Arachidonic Acid
Brain
Carcinogens
Cell Differentiation
Cell Division
Cell Line
Dose-Response Relationship, Drug
Enzyme Activation
Humans
Kinetics
Leukemia, Promyelocytic, Acute
Lipid Bilayers
Macrophages
Mice
Mice, Inbred BALB C
Monocytes
Phorbol 12,13-Dibutyrate
Phosphorylation
Plasmacytoma
Protein Binding
Protein Kinase C
Rats
Subcellular Fractions
Terpenes
Tumor Cells, Cultured