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Modulation of the Growth of a Human Erythroleukemic Cell Line (K562) by Prostaglandins: Antiproliferative Action of Prostaglandin A¹

Institute of Experimental Medicine, C. N. R., II University of Rome, Via O. Raimondo, 00173 Rome [M. G. S., A. C.], and Center of Virology, Osp. S. Camillo, C. Gianicolense 85, 00152 Rome [A. B., C. A.], Italy

Among several prostaglandins (PGs) tested, PGF₁ 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 ,ß-unsaturated carbonyl group in the cyclopentane ring are potential antineoplastic agents.

¹ This work was partially supported by a grant from the National Council of Research of Italy, P. F. "Control of Infectious Diseases," No. 8403243.

² To whom requests for reprints should be addressed.

Received 3/13/86. Revised 8/ 1/86. Accepted 8/14/86.

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