Knockdown Of FOXK1 Inhibited The Proliferation,Migration And Invasion In Hepatocellular Carcinoma Cells

Objection: Hepatocellulor carcinoma(HCC)is common malignancy and the treatment is always a challenging.The biology mechanism of the development of is not so clear to date.Gene fork head box k1(FOXK1)is a member of the FOX transcription factors family,and plays critical roles in the development of many types of human cancers.However,the biological function of FOXK1 in HCC has not been explored.This study aims to investigate the function of FOXK1 in the development of human HCC and its possibility as a potential therapeutic target.Methods: The expression of FOXK1 in human tissues(10 patients with HCC,tumor tissues and adjacent liver tissues)HCC cell lines(Hep G2,HCCLM3 and Hep3B)and normal liver HL-02 cell lines)were detected by real time PCR and western blot.The expression of C-MYC,Cyclin D1 and the biological ability of cell invasion and migration in vito,and tumorigenesis in vivo were evaluated after FOXK1 knocked down in HCC cell lines by sh RNA.Results: FOXK1 is over expressed in human HCC tissues and HCC cell lines.Knock down of FOXK1 in HCC cell lines decreased the expression of ?-catenin,C-MYC and Cyclin D1,and inhibited the proliferation,invasion and migration in vitrol and tumorigenesis in vivo.Inhibition of Wnt/?-catenin signaling pathway partly reversed the decreased proliferation and invasion of Hep G2 by knocking down of FOXK1.Conclusion: FOXK1 promotes the development of HCC throwgh activating Wnt/?-catenin signaling pathway,and FOXK1 is a potential molecular target for HCC treatment.