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Studies on the Interaction between Interleukin 6 and Human Malignant Nonhematopoietic Cell Lines¹

Division of Hematology and Oncology, Department of Medicine I, Technische Universitaet of Munich, Munich [H. S., G. S., D. O., W. E. B.], and Department of Transfusion Medicine, University of Ulm, German Red Cross Blood Center, Ulm [W. A. F., H. N.], Federal Republic of Germany

We have previously reported on stimulation of clonal growth of cell lines from human solid tumors by recombinant human interleukin 3, recombinant human granulocyte-macrophage colony-stimulating factor, and recombinant human granulocyte colony-stimulating factor (W. E. Berdel et al., Blood, 73: 80–83, 1989; Exp. Hematol., 16: 510, 1988). Within an extensive screening program of hematopoietic growth factor activity on malignant cells, the effects of recombinant human interleukin 6 (rhIL-6) were tested on the growth (tritiated thymidine uptake and human tumor cloning assay) of 26 different human cell lines derived from a wide range of solid tumors (head and neck, 4; lung, 1; pancreatic, 1; gastric, 1; colorectal, 3; renal, 3; bladder, 1; prostate, 1; breast, 2; ovary, 2; choriocarcinoma, 1; sarcoma, 2; glioblastoma, 2; neuroblastoma, 2). rhIL-6 (dose range up to 10⁴ IU/ml) caused no reproducible enhancement or inhibition of tritiated thymidine uptake by tumor cell lines from nonhematopoietic origin. Furthermore, 19 of the tumor cell lines were clonogenic in a capillary modification of the human tumor cloning assay. No reproducible stimulation of clonal growth by rhIL-6 was observed in any of the cells tested. Particularly, there was no sensitivity of those cell lines for rhIL-6, which were previously shown to be sensitive for recombinant human interleukin 3 and recombinant human granulocyte-macrophage colony-stimulating factor in this assay. On the other hand, there were no significant growth-inhibitory effects of rhIL-6 on the cell lines tested in this study. Further experiments showed no influence of neutralizing monoclonal anti-hIL-6 antibody on the growth of 3 kidney carcinoma cell lines, making autocrine growth-modulating loops for IL-6 in these lines unlikely. In conclusion, no major interactions between hIL-6 and the growth of the human malignant cell lines from nonhematopoietic origin tested were detected in this study.

¹ This work was supported by a grant from Deutsche Forschungsgemeinschaft (DFG Be 822/4-2).

² Recipient of a Heisenberg-Scholarship of the Deutsche Forschungsgemein-schaft. To whom requests for reprints should be addressed, at Department of Hematology and Oncology, Klinikum Steglitz, Freie Universitaet Berlin, Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany.

Received 7/17/91. Accepted 5/17/91.

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