KDM6A promotes hepatocellular carcinoma progression and dictates lenvatinib efficacy by upregulating FGFR4 expression
Description
Hepatocellular carcinoma (HCC) is one of major causes of death from cancer and has a very poor prognosis with few effective therapeutic options. Despite the approval of lenvatinib for the treatment of patients with advanced HCC, only a few of patients can benefit from this targeted therapy. Our study revealed that KDM6A is significantly upregulated in HCC and is associated with a poor prognosis. Hepatic Kdm6a loss also inhibited liver tumorigenesis in a mouse liver tumor model. Mechanistically, KDM6A loss downregulated the FGFR4 expression to suppress the PI3K-AKT-mTOR signaling pathway, leading to a glucose and lipid metabolism reprogramming in HCC.
