Growth-stimulating activity of interleukin 6 on human mammary epithelial cells transfected with the int-2 gene.

We have shown recently that normal human mammary epithelial cells do produce interleukin 6 (IL6), interleukin 8, and a nonsecreted form of tumor necrosis factor. Here we report that ductal infiltrating mammary carcinomas fail to express immunoreactive IL6. Since abnormalities of cytokine genes are a frequent event in cancer, we investigated the production of and the response to cytokines of mammary cells using a panel of oncogene-transformed cells derived from the spontaneously immortalized MCF-10A cell line. We found that only the parental line and the int-2-transformed cells responded to exogenous IL6 and/or were suppressed by IL6-neutralizing antibody. In contrast to highly transformed cells, these two lines, which were either nontransformed (MCF-10A) or weakly transformed (int-2), were found to express IL6 receptors. These data suggest that loss of IL6 pathways can be a marker of mammary cell transformation.