Fatty acid regulation of protein kinase C isoforms in prostate cancer cells

Polyunsaturated fatty acids influence the aetiology of prostate cancer. The ir effects on cellular mechanisms regulating prostate tumorigenesis are unc lear. Using prostate cancer cells (LNCaP), we determined effects of n-9-OA, n-6-LA, and n-3-EPA on total PKC and its isoforms in relation to cell prol iferation and PSA production. PKC-alpha, delta, gamma, iota, mu, and zeta w ere present in LNCaP cells; PKC-beta, epsilon, eta, and theta isoforms were not. PKC-alpha was detected only in cytosol; PKC-delta, iota, gamma, and m u were present in cytosol and in membranes. Fatty acids increased cell prol iferation, total PKC activity and elicited pro-proliferative effects on spe cific PKC isoforms (PKC-delta and -iota). EPA and LA increased total PKC ac tivity and reduced membrane-abundance of PKC-delta. OA reduced cytosolic an d membrane PKC-delta. Only EPA reduced PKC-gamma membrane abundance. Fatty acids enhanced cytosolic PKC-iota abundance but only EPA and to a lesser ex tent LA increased its membrane content. Changes in PKC-delta, -iota, and -g amma did not affect PSA production. (C) 2001 Academic Press.