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Interleukin 6 Stimulates the Production of Immunoreactive Endothelin 1 in Human Breast Cancer Cells

Department of Surgery II, Kumamoto University Medical School, Honjo 1-1-1, Kumamoto 860 [J-i. Y., M. O., K. N., S. M., K. I., S-i. Y., Y. N., T. S., S. T.], and Kitazato Biochemical Laboratories, Kitazato 1-15-1, Sagamihara, Kanagawa 228 [S. F.], Japan

To investigate the potential regulation of endothelin 1 production in human breast cancer cells, we measured the release of immunoreactive endothelin 1 (ir-ET-1) from the MCF-7 and ZR-75-1 breast cancer cell lines in response to various agents including estrogen and tamoxifen as well as several cytokines. ir-ET-1 was detected in conditioned medium of MCF-7 cells and ZR-75-1 cells by specific radioimmunoassay. Among the agents tested, estrogen, tamoxifen, tumor necrosis factor, -interferon, interleukin (IL) 1, and transforming growth factor ß had no effect on ir-ET-1 secretion by these breast cancer cells. However, IL-6 (20 ng/ml) treatment of MCF-7 cells and ZR-75-1 cells caused maximal increases in the amount of ir-ET-1 secreted into the culture medium to 206 and 314% of basal values after 6 h, respectively. This effect of IL-6 on ir-ET-1 secretion was inhibited by actinomycin D and cycloheximide, indicating that IL-6 stimulates de novo synthesis of ir-ET-1 at a transcriptional level. Reverse-phase high performance liquid chromatography coupled with radioimmunoassay in the conditioned medium from IL-6-treated cells revealed one major ir-ET-1 component corresponding to human standard ET-1. The present study demonstrates the potential for IL-6 to stimulate ir-ET-1 production in human breast cancer cells, which may participate in the process of acute phase reactant-like expression of this peptide and/or in the process of IL-6 enhanced breast cancer cell motility, the latter being recently clarified.

¹ To whom requests for reprints should be addressed.

Received 10/20/92. Accepted 12/14/92.

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