Overexpression of IL-6 and STAT3 May Provide New Insights into Ovine Pulmonary Adenocarcinoma Development

Background Ovine pulmonary adenocarcinoma (OPA) is caused by Jaagsiekte sheep retrovirus (JSRV) and is considered the most suitable animal model for human lung cancer. The precise mechanisms of OPA oncogenesis are still uncertain. Signal transducer and activator of transcription 3 (STAT3) is activated by interleukin-6 (IL-6) in many cancers, but this aspect is unknown in OPA. We aimed to evaluate the expression of IL-6 and STAT3 in OPA for its potential role in pulmonary carcinogenesis. Results Twenty cases of JSRV-positive OPA and 9 normal lung tissues from sheep were included in the study. Tissue samples were stained with antibodies for IL-6, STAT3, and JSRV-MA. IL-6 and STAT3 were semi-quantified in OPA and control groups using Western Blot (WB). IL‑6 was expressed in stromal, inflammatory, and epithelial cells in all cases of OPA, while STAT3 expression was restricted to epithelial cells. In the OPA group, the percentage of immunolabelled cells for STAT3 accounted for a mean value of 96%. Using the H-SCORE method, 95% of cases were considered positive for STAT3 expression. Control tissuesshowed multifocal andweak immunoexpression for both markers. Using WB analysis, a highly significant amount of both IL-6 (p=0.0078) and STAT3 (pConclusions Our data showed overexpression of IL-6 and STAT3 in OPA in comparison with healthylungs. These results suggest a potential role of IL6-STAT3 in OPA carcinogenesis.