A23187 and protein kinase c activators stimulate phosphatidylinositol metabolism and prostaglandin synthesis in a human lung cancer cell line Academic Article Article uri icon


MeSH Major

  • Macula Lutea
  • Retinal Diseases


  • Activation of cell phospholipase, release of arachidonic acid and stimulation of prostaglandin synthesis were studied in a newly described human tumor cell line (Lu-65). In the Lu-65 tumor cell line, the calcium ionophore A23187 (2 microM) caused a 100% increase in the release of 3H-arachidonic acid and a 7-fold increase in the synthesis of prostaglandin E2. 1-oleoyl, -2-acetyl-glycerol (100 microM) increased arachidonate release and prostaglandin E2 synthesis by 100%. A23187 and the protein kinase C activators, 1,2-dioctanoyl-glycerol and 1-oleoyl, -2-acetyl-glycerol, decreased the specific radioactivity of 3H-arachidonate in phosphatidylinositol by 37% and 57%, respectively. The effects of A23187 were blocked in Ca2+-free media or in the presence of the phospholipase A2 inhibitor, p-bromophenacyl bromide, while those of 1-oleoyl, -2-acetyl-glycerol were not. The data provide evidence in a human tumor cell line for calcium/phospholipase A2-dependent and independent pathways for arachidonic acid release, both of which preferentially hydrolyze phosphatidylinositol.

publication date

  • October 31, 1988



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1016/S0006-291X(88)80891-X

PubMed ID

  • 3142461

Additional Document Info

start page

  • 644

end page

  • 52


  • 156


  • 2