YAP-induced MAML1 cooperates with STAT3 to drive hepatocellular carcinoma progression.

ABSTRACT: Hepatocellular carcinoma (HCC) is a major liver malignancy and a leading cause of cancer-related mortality worldwide. Given its rising incidence and poor prognosis, there is an urgent need to elucidate the molecular mechanisms driving HCC progression and to develop novel targeted therapies. In this study, we identify MAML1 as a key contributor to HCC development. Elevated MAML1 expression strongly correlated with disease severity, whereas its knockdown suppressed HCC progression. Functionally, MAML1 promoted tumor malignancy by regulating STAT3 activity. Mechanistically, MAML1 interacted with STAT3 and enhanced its acetylation in a p300-dependent manner. Inhibition of STAT3 with a specific inhibitor attenuated MAML1-driven HCC progression. Furthermore, signaling pathway analyses revealed t

SUBMITTER: Li J 

PROVIDER: S-EPMC12696947 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature