FAM188B promotes progression of hepatocellular carcinoma by regulating YAP/TAZ via interaction with USP10

objectives Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and its incidence and mortality rates remain high. Therefore, new diagnostic and therapeutic approaches are urgently required. FAM188B mRNA encodes an evolutionarily conserved protein that is highly expressed in various cancers. While FAM188B has been implicated in the progression of several tumors, its role in HCC progression remains unknown. Methods We analyzed FAM188B expression in HCC using TCGA and UALCAN databases. Functional studies included in vitro proliferation, migration, and invasion assays, as well as in vivo xenograft models. Co-immunoprecipitation (Co-IP), Western blotting, and immunofluorescence were used to investigate the FAM188B-USP10-YAP/TAZ interaction. Results FAM188B was found highly expressed in HCC cells and associated with poor prognosis. Both in vitro and in vivo, FAM188B promoted the proliferation, migration, and invasion of HCC. FAM188B directly interacts with and stabilizes USP10 and the downregulation of FAM188B by shRNA led to decreased USP10 and YAP/TAZ protein levels, suggesting that FAM188B may regulate the YAP/TAZ pathway through its interaction with USP10. Conclusion This study suggests that FAM188B is involved in the proliferation, migration and invasion of hepatocellular carcinoma (HCC) and the mechanism may involve the regulation of the USP10/YAP/TAZ signalling pathways in vitro and in vivo.