Abstract
Adherent B16 amelanotic melanoma (B16a) cells exposed to fatty acid 12(S)-HETE, a lipoxygenase metabolite of arachidonic acid, demonstrated a gradual dissolution of stress fibers and bundling-together of vimentin. The 12(S)-HETE effects on tumor cell cytoskeleton appeared 5 min after treatment, became prominent -15 min following stimulation, and generally disappeared by 30 min. Simultaneous treatment of cells with 12(S)-HETE and okadaic acid (OA) prevented disappearance of the 12(S)-HETE effects by 30 min. Quantitative double immunoblotting of actin and vimentin indicated that actin, but not vimentin, underwent a time-related depolymerization. On the other hand, enhanced phosphorylation of vimentin but not of actin was observed after 12(S)-HETE treatment. 12(S)-HETE-enhanced vimentin phosphorylation was abolished by protein kinase C (PKC) inhibitor calphostin C., thus suggesting the involvement of PKC.
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Tang, D.G., Honn, K.V. (1997). Role of Protein Kinase C and Phosphatases in 12(S)-Hete-Induced Tumor Cell Cytoskeletal Reorganization. In: Honn, K.V., Nigam, S., Marnett, L.J. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 2. Advances in Experimental Medicine and Biology, vol 400. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5325-0_48
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DOI: https://doi.org/10.1007/978-1-4615-5325-0_48
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