IL-23/IL-23R: potential mediator of intestinal tumor progression from adenomatous polyps to colorectal carcinoma

Purpose Interleukin 23 (IL-23) affects tumor growth by regulating Th cells and plays a vital role in immunosuppression in tumor tissues. However, whether tumor cells are IL-23R positive or whether IL-23 has the potential to influence the growth of cancer cells directly remains unclear. The aim of this study was to clarify the molecular expression patterns of IL-23, IL-23R, and Forkhead box P3 (FOXP3) in normal tissues adjacent to cancer, in intestinal polyps (IP), and in colorectal carcinoma (CRC), and to infer the relationship between the expression patterns of these three molecules and the progress of intestinal tumors from adenomatous polyps to colorectal cancer. Methods The levels of IL-23A, IL-23R, and FOXP3 were evaluated in normal tissues adjacent to cancer (NT, n = 13), IP (n = 26), and CRC (n = 13) using real-time PCR, ELISA, western blotting, immunohistochemistry, and immunocytochemistry. Results The expression of IL-23 and FOXP3 increased progressively from NT through to CRC. Immunohistochemistry staining showed that IL-23R was highly positive in carcinoma cells of the CRC group, whereas it was partially positive in cells of other groups. In addition, the human CRC cell line SW-480 exhibited weak IL-23R immunocytochemical positivity. Conclusions We propose that the IL-23/IL-23R pathway is a potential route to facilitate the malignant progression of cancers. The relationship between IL-23 and FOXP3 in the microenvironment of carcinoma led us to deduce that these two molecules may interact with each other. Although the exact mechanism underlying this interaction remains a mystery, we are convinced that these two molecules are relevant in cancer progression and that IL-23 could be a potential target for cancer immunotherapy.