Chronic infection with hepatitis B virus (HBV) is one of the major risk factors for
hepatocellular carcinoma. HBV
infection can induce the expression of
IL-23. However, the effects of
IL-23 on
carcinogenesis are rare and contradictory. To investigate the potential role of
IL-23 on malignant properties of
hepatoma cells, in the present study, first, we confirmed that HBV drove infected
hepatoma cells to produce more
IL-23. And then we found that at low concentration, human recombinant
IL-23 (hrIL-23) enhanced malignant properties of
hepatoma cells through increasing the proportion of stem/progenitor cells, promoting proliferation and colony formation, reducing apoptosis and inducing motility and invasivity of them.
Hepatocyte nuclear factor 4 alpha (HNF4α), which is essential for liver development and hepatocyte function, was found to be downregulated in HBV integrated or transiently transfected
hepatoma cells. Its expression was also decreased in cells treated by hrIL-23 or by HepG2.215 culture supernatant and this decrease could be abolished by supplementation of anti-IL-23p19 antibody. Hence, it is speculated that HBV related
IL-23 can enhance malignant properties of
hepatoma cells through attenuation of HNF4α. The findings identified a potential target of interventional strategies for treating
hepatitis B patients through manipulation of the
IL-23.