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Previous studies have indicated that FoxP1, FoxP2 and FoxP3 play important roles in hepatocellular carcinoma (HCC). However, the effect of FoxP4 in HCC requires further elucidation. The aim of the present study was to explore the roles of FoxP4 in HCC and further decipher the detailed mechanism. In present study, it was found that FoxP4, which is overexpressed in HCC tissues and cell lines, facilitated EMT in HCC cell lines through regulation of Slug. First, increased expression of FoxP4 was identified in 110 pairs of human HCC tumor and their adjacent normal tissues. In addition, the association between FoxP4 expression and clinicopathological features of HCC patients indicated that FoxP4 played vital roles in HCC development. Subsequently, gain- and loss-of-function experiments indicated that FoxP4 promoted cellular proliferation, migration as well invasion. In addition, EMT, a key mechanism during cancer metastasis, was regulated by FoxP4. Furthermore, ChIP and qChIP as well as luciferase reporter assays indicated that Slug, an EMT-associated transcription factor, was transcriptionally regulated by FoxP4. In conclusion, FoxP4 functioned as a tumor promoter in HCC cells by transcriptionally regulating Slug, and the present study highlighted the potential effects of FoxP4 on the prognosis and treatment of HCC.

Upregulation of FoxP4 in HCC promotes migration and invasion through regulation of EMT