FAIM modulates HCC progression via enhancing HMGA1 interaction with CDK7 and promoting its phosphorylation level.

ABSTRACT:

Background

Hepatocellular carcinoma (HCC), characterized by its aggressive trait and rapid progression, stands as one of the leading causes of cancer-related death worldwide. Fas apoptotic inhibitory molecule (FAIM), a death receptor antagonist, impedes cell apoptosis by reinforcing protein phosphorylation and stability. High mobility group A1 (HMGA1) is reported to be subject to multiple posttranslational modification, and plays a crucial role in HCC development. However, whether FAIM facilitates tumorigenesis through modulating HMGA1 phosphorylation remains unclear.

Methods

We applied Huh7 and SNU387 cells to investigate the regulatory role of FAIM in cell proliferation and apoptosis. Next, we constructed a male BALB/C mouse model with HCC to explore the biological functio

SUBMITTER: Li Y 

PROVIDER: S-EPMC12522979 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature