This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kilian, P. L. Articles by Campen, C. A. Search for Related Content PubMed PubMed Citation Articles by Kilian, P. L. Articles by Campen, C. A.

Antiproliferative Effect of Interleukin-1 on Human Ovarian Carcinoma Cell Line (NIH:OVCAR-3)

Departments of Immunopharmacology [P. L. K., K. L. K, D. A. B., W. R. B., C. A. C] and Investigative Toxicology [J. M. L., D. F.], Hoffmann-La Roche Inc., Nutley, New Jersey 07110

The human ovarian carcinoma cell line, NIH:OVCAR-3, possesses high affinity receptors for interleukin-1 (IL-1). Binding experiments with ¹²⁵I-IL-1 indicate a dissociation constant of approximately 55 pM and the presence of approximately 7800 receptors/cell. These receptors bind both IL-1 and IL-1ß and internalize IL-1. Proliferation of NIH:OVCAR-3 cells is inhibited by IL-1. Half-maximal inhibition is observed with 2–3 units/ml of IL-1 or IL-1ß. A maximal effect (80% inhibition of cell proliferation) is achieved by treatment of cells with 10 units/ml of IL-1 for 3 days. The antiproliferative effect of IL-1 is blocked by IL-1 receptor antagonist. Light and electron microscopy studies show that IL-1 treatment causes cytopathological changes and a reduction in the number of mitotic figures in NIH:OVCAR-3. IL-1 stimulates prostaglandin E₂ release by NIH:OVCAR-3 cells, but this response is unrelated to the antiproliferative effect of IL-1. Interferon- A (IFN- A) also inhibits growth of NIH:OVCAR-3 cells in a concentration-dependent manner. Combination of IFN- A and IL-1 gives synergistic inhibition of NIH:OVCAR-3 cell proliferation. IL-1 alone or in combination with IFN- A or other agents may be useful for treatment of human ovarian cancer.

¹ To whom requests for reprints should be addressed, at Department of Immunopharmacology, Hoffmann-La Roche Inc., Building 86, Nutley, NJ 07110.

² Present address: Department of Reproductive Endocrinology, The R. W. Johnson Pharmaceutical Research Institute, Raritan, NJ 08869.

Received 10/ 8/90. Accepted 1/21/91.

This article has been cited by other articles:

				L. A. Hefler, E. Ludwig, A. Lebrecht, R. Zeillinger, D. Tong-Cacsire, H. Koelbl, S. Leodolter, and C. B. Tempfer Polymorphisms of the Interleukin-1 Gene Cluster and Ovarian Cancer Reproductive Sciences, November 1, 2002; 9(6): 386 - 390. [Abstract] [PDF]

				S. Muthukkumar, S. F. Sells, S. A. Crist, and V. M. Rangnekar Interleukin-1 Induces Growth Arrest by Hypophosphorylation of the Retinoblastoma Susceptibility Gene Product RB J. Biol. Chem., March 8, 1996; 271(10): 5733 - 5740. [Abstract] [Full Text] [PDF]

				E. I. Deryugina and M. A. Bourdon Tenascin mediates human glioma cell migration and modulates cell migration on fibronectin J. Cell Sci., March 1, 1996; 109(3): 643 - 652. [Abstract] [PDF]

				T. Murai, Y. Nakagawa, H. Maeda, and K. Terada Altered Regulation of Cell Cycle Machinery Involved in Interleukin-1-induced G1 and G2 Phase Growth Arrest of A375S2 Human Melanoma Cells J. Biol. Chem., February 23, 2001; 276(9): 6797 - 6806. [Abstract] [Full Text] [PDF]