Combination of TNFα / IFNγ Induces Apoptosis and IL-32 Expression in Human Colon Cancer Cell Line HCT116

Chronic inflammatory diseases such as Crohn′s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma. Apoptic induction of colon cancer cell by cytokines and death receptors is one of important anti-cancer therapies. We observed that human colon cancer cell line, HCT116, was induced cell death and IL-32 expression by co-administration of TNFα and IFNγ. Cleavage forms of caspase-3, caspase-9 and PARP were increased in TNFα / IFNγ-treated HCT116. mRNA expression of death receptors including TNFR1 and Fas were not changed and NO generation was not induced by combination of TNFα and IFNγ. But mRNA expression of IL-32α, β and γ were increased in TNFα / IFNγ-treated HCT116. To determine effect of IL-32 in HCT116 cell apoptosis by TNFα / IFNγ stimulation, IL-32 siRNA-transfected HCT116 cell were cultured with TNFα / IFNγ and cells proliferation was measured. IL-32 siRNA slightly recovered cell viability of TNFα / IFNγ-stimulated HCT116. These results suggest that IL-32 not directly related to apoptosis of HCT116 by TNFα / IFNγ stimulation. But IL-32 expression by TNFα or TNFα / IFNγ in colon cancer cell line is very interesting because of unknown effect of IL-32 in colon cancer. Our study will contribute to development of studies for IL-32 function in human colon cancer and anti-cancer therapies using cytokines.