Modulation of the growth of a human erythroleukemic cell line (K562) by prostaglandins: antiproliferative action of prostaglandin A.
Among several prostaglandins (PGs) tested, PGF1 alpha was found to slightly enhance, while PGAs and PGDs were found to drastically inhibit the growth of K562 cells in culture. This effect was dose dependent. While PGD2 was cytotoxic, PGA1 treatment could totally inhibit K562 cell proliferation, without affecting cell viability. PGA1 action was reversible; however, K562 cells totally lost their growth potential after prolonged exposure to PGAs. While it did not significantly affect DNA and RNA synthesis, PGA1 partially inhibited protein synthesis and glycosylation in these cells. In particular, the production of two polypeptides with molecular weights of 92,000 and 46,000, respectively, was decreased, while the synthesis of a protein with a molecular weight of 74,000 was induced. These results strongly support the concept that PGs are involved in the regulation of cell proliferation, and that PGs containing a reactive alpha, beta-unsaturated carbonyl group in the cyclopentane ring are potential antineoplastic agents.
D003994:Bucladesine / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D004247:DNA / Q000096:biosynthesis; D006801:Humans; D004915:Leukemia, Erythroblastic, Acute / Q000378:metabolism / Q000473:pathology*; D011453:Prostaglandins / Q000494:pharmacology; D011454:Prostaglandins A / Q000494:pharmacology*; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis
D011453:Prostaglandins; D011454:Prostaglandins A; D012313:RNA; D003994:Bucladesine; D004247:DNA; C100573:prostaglandin A1