Oka M, Iizuka N, Yamamoto K, Gondo T, Abe T, Hazama S, Akitomi Y, Koishihara Y, Ohsugi Y, Ooba Y, Ishihara T, Suzuki T
Department of Surgery II, Yamaguchi University School of Medicine, Japan.
J Interferon Cytokine Res. 1996 Dec;16(12):1001-6. doi: 10.1089/jir.1996.16.1001.
We reported that human esophageal cancer cell lines (ECC) (YES-1, -2, -3, -4, -5, and -6) produced interleukin-6 (IL-6). We, therefore, investigated the growth effects ([3H]thymidine uptake assay and direct cell count) of IL-6 on these ECC. IL-6 receptor (R) and GP-130 mRNA were detected in all the ECC, using reverse transcriptase-polymerase chain reaction (RT-PCR) assay, and IL-6R was detected in one (YES-3) by immunohistochemical staining. IL-6, anti-IL-6 monoclonal antibody (mAb), or anti-IL-6R mAb caused no reproducible enhancement or suppression of [3H]thymidine uptake by all six ECC. Direct cell count also revealed that the growth enhancement or suppression by IL-6, anti-IL-6 mAb, or anti-IL-6R mAb was relatively small. Particularly, there was no significant sensitivity of YES-3 cells, which definitely produce IL-6 and express IL-6R for IL-6, anti-IL-6 mAb, or anti-IL6R mAb. These results suggest that some esophageal cancers may produce IL-6 and express IL-6R. However, no major interactions between IL-6 and the growth of human esophageal cancer cell lines were detected in this study.
