Dual effect of the phorbol ester TPA on arachidonic acid release from HeLa cells

FEBS Letters

Espe, U.²  Kinzel, V.²  Fu¨rstenberger, G.¹  Kaszkin, M.² 

[1] Biochemistry, German Cancer Research Center, Im Neuenheimer Feld 280, 6900 Heidelberg, FRG;Institutes of Experimental Pathology, German Cancer Research Center, Im Neuenheimer Feld 280, 6900 Heidelberg, FRG

关键词: Tumor promoter;    Phospholipid metabolism;    Phospholipase A2;    Arachidonic acid;    AA;    arachidonic acid;    CH;    cycloheximide;    PGE2;    prostaglandin E2;    PLA2;    phospholipase A2;    PC;    phosphatidylcholine;    PE;    phosphatidylethanolamine;    PI;    phosphatidylinositol;    PS;    phosphatidylserine;    TPA;    12-O-tetradecanoylphorbol 13-acetate;   

DOI  :  10.1016/0014-5793(88)80435-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) induces release of arachidonic acid (AA) from HeLa cells with a maximum at 2–3 h. Subsequently the extracellular level of AA decreases. Cycloheximide (CH, 10⁻⁵ M) does not influence the release of AA, however, it causes the AA level to remain elevated. In the presence of TPA and CH (i) re-uptake of AA is not altered, (ii) re-incorporation of AA into phosphatidylinositol (and phosphatidylethanolamine) is largely increased, and (iii) the level of lysophosphatidylinositol is elevated. The latter two phenomena can be prevented by fluocinolone acetonide (10⁻⁸ M), i.e. by inhibition of phospholipase A₂ (PLA₂). These data point to a continuously elevated PLA₂ activity in the presence of TPA and CH. The phorbol ester appears to induce a proteinaceous principle which diminishes PLA₂ activity.

【 授权许可】

Unknown