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Interleukin (IL)-27, composed of p28 and Epstein-Barr virus-induced gene3 (EBI3) subunits, has diverse functions in regulating immune systems. Human melanomacells have been shown to express both IL-27 receptor subunits, and growth inhibitionby IL-27 was detected. We investigated whether forced expression of the p28-linkedEBI3 gene in human pancreatic carcinoma cells (AsPC1) by retroviral vector wouldproduce IL-27-mediated antitumor effects and the related mechanisms. The datademonstrated that AsPC1 cells expressed both IL-27 receptor subunits, and tumorgrowth of AsPC1/IL-27 in mice was retarded compared with vector DNA-transducedtumors and survival of the mice was prolonged. Expression of cytokines such asinterferon-γ, tumor necrosis factor-α and IL-1β in tumor specimens increased,while the secretion of IFN-γ and TNF-α from spleen cells of mice bearing IL-27-transfectedtumors increased. Moreover, cell cycle arrest was induced in AsPC1/IL-27 inoculatedmice with upregulated p21 expression and downregulated survivin expression. Theappearance of apoptotic cells increased in tumor specimens of mice bearing IL-27-transfectedtumors compared with the mice bearing DNA-transfected tumors by confirming theexpression of apoptosis-related proteins and activated apoptotic pathways throughdetection of cleaved PARP. These results suggest that transfection of the IL-27gene into human pancreatic carcinoma cells could produce antitumor effects in vivoand induction of cell cycle arrest and apoptosis could be the mechanism of IL-27action in tumor regression.

oncology reports

Effects on apoptosis and cell cycle arrest contribute to the antitumor responses of interleukin-27 mediated by retrovirus in human pancreatic carcinoma cells