Fatty Acid Regulation of Protein Kinase C Isoforms in Prostate Cancer Cells

S.S. Pandian, Alan Arthur Sneddon, Charles Bestwick, S. McClinton, , I. Grant, Klaus Wilfried Juergen Wahle, S.D. Heys

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


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 languageEnglish
Pages (from-to)806-812
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 18 May 2001


  • fatty acids
  • prostate cancer
  • protein kinase C
  • prostate specific antigen
  • Phorbol ester
  • nude-mice
  • in-vitro
  • growth
  • tumor
  • involvement
  • expression
  • apoptosis
  • carcinoma
  • membrane


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