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Background  Tumor progression locus 2 (TPL2), a serine-threonine kinase, functions as a critical regulator of inflammatory pathways and mediates oncogenic events. The potential role of  Tpl2  in nonalcoholic fatty liver disease (NAFLD) associated hepatocellular carcinoma (HCC) development remains unknown.    Methods  Both wild-type and  Tpl2  knockout male mice were initiated by a hepatic carcinogen (diethylnitrosamine, i.p. with a single dose of 25 mg.kg −1 )at 2 weeks of age, and then were given the high carbohydrate diet feeding to induce hepatic steatosis, inflammation, adenoma and HCC for 24 weeks.    Results   Tpl2  knockout mice had significantly lower incidences of liver tumor and developed hepatocellular adenoma only, which is contrast to wild-type mice where they all developed HCC.  Tpl2  knockout mice had significantly down-regulated phosphorylation of JNK and ERK, and levels of mRNA expression of pro-inflammatory cytokines ( Il-1β, Il-18, Mcp-1  and  Nalp3 ), which correlated with the reduced incidence and number of hepatic inflammatory foci. Furthermore,  Tpl2  ablation resulted in decreased hepatic steatosis and expression of de novo lipogenesis related markers (ACC, SCD1, SREBP1C and AKT phosphorylation), as well as reduction of endoplasmic reticulum stress biomarkers PERK and eIF-2a.    Conclusion  The study revealed for the first time that  Tpl2  plays a significant role in promoting HCC development by its pro-inflammatory effect, which suggested that  Tpl2  could be a molecular target for HCC prevention.

Tumor progression locus 2 ablation suppressed hepatocellular carcinoma development by inhibiting hepatic inflammation and steatosis in mice