Abstract
Polyunsaturated fatty acids influence the aetiology of prostate cancer. Their effects on cellular mechanisms regulating prostate tumorigenesis are unclear. 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 proliferation and PSA production. PKC-alpha, delta, gamma, iota, mu, and zeta were 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 mu were present in cytosol and in membranes. Fatty acids increased cell proliferation, total PKC activity and elicited pro-proliferative effects on specific PKC isoforms (PKC-delta and -iota). EPA and LA increased total PKC activity and reduced membrane-abundance of PKC-delta. OA reduced cytosolic and membrane PKC-delta. Only EPA reduced PKC-gamma membrane abundance. Fatty acids enhanced cytosolic PKC-iota abundance but only EPA and to a lesser extent LA increased its membrane content. Changes in PKC-delta, -iota, and -gamma did not affect PSA production. (C) 2001 Academic Press.
Original language | English |
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Pages (from-to) | 806-812 |
Number of pages | 7 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 283 |
Issue number | 4 |
DOIs | |
Publication status | Published - 18 May 2001 |
Keywords
- fatty acids
- prostate cancer
- protein kinase C
- prostate specific antigen
- Phorbol ester
- nude-mice
- in-vitro
- growth
- tumor
- involvement
- expression
- apoptosis
- carcinoma
- membrane