MTDH-stabilized DDX17 promotes tumor initiation and progression through interacting with YB1 to induce EGFR transcription in Hepatocellular Carcinoma

This study identified DDX17 as a novel binding partner of MTDH. Furthermore, MTDH increased the protein level of DDX17 by inhibiting its ubiquitination. The increased expression of DDX17 was closely associated with vascular invasion, TNM, BCLC, and poor prognosis. In vitro and in vivo tests demonstrated that DDX17, a downstream target of MTDH, played a crucial role in tumour initiation and progression. This, in turn, increased expression of EGFR and the activation of the downstream MEK/pERK signalling pathway. The results identify DDX17, stabilized by MTDH, as a potent oncogene in HCC and suggest that the DDX17/YB1/EGFR axis contributes to tumorigenesis and metastasis of HCC.