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Effect of Doxorubicin on Mouse Hybridoma B Cells: Stimulation of Immunoglobulin Synthesis and Secretion¹

Laboratoire d'Immunologie Cellulaire et Clinique, INSERM U.255, Institut Curie, 75005 Paris, France [J. L. T., W. H. F.] and Laboratoire de Pharmacologie Cellulaire et Moléculaire, CNRS UA 04-1163, ICIG, Hôpital Paul Brousse, 94800 Villejuif, France [A. F., J. H., H. T.]

The purpose of these studies was to investigate whether the cell-differentiating effect of anthracyclines can trigger an over-production and secretion of molecules that may interfere with the tumor-host relationship. We exposed mouse hybridoma B-cells, which are devoted to immunoglobulin production, to doxorubicin (10–40 ng/ml). We found that most doxorubicin-treated cells secreted 3- to 5-fold higher amounts of immunoglobulin than untreated cells, along with an accumulation of 50% of them in the G2+M phase of the cell cycle. The antigenic specificity of the immunoglobulin and its size pattern as determined by polyacrylamide gel electrophoresis were similar whether or not cells were treated with doxorubicin. The enhancement of immunoglobulin secretion by doxorubicin was associated with an increase of the intracellular pool of heavy and light chains of the immunoglobulin. Furthermore, an elevated synthesis of immunoglobulin was observed. The synthesis of other proteins also appeared to be modified in these circumstances. These data suggest that doxorubicin can potentiate the biological functions of target cells when used at low concentrations, elevating the production and secretion of effector molecules that interfere with the tumor-host relationship.

¹ This research was supported by Institut National de la Santé et de la Recherche Médicale, Institut Curie, and by grants from the Ligue Nationale contre le Cancer, Fondation contre la Leucémie/Fondation de France, and the Association de la Recherche contre le Cancer.

² To whom requests for reprints should be addressed, at INSERM U.255, Institut Curie, 26 rue d'Ulm, 75231 Paris-Cedex 05, France.

Received 10/26/88. Revised 5/22/89. Accepted 6/13/89.