NOP56 interacts with Fibrarin to regulate the PI3K/AKT signaling pathway and inhibit apoptosis of hepatocellular carcinoma.

ABSTRACT:

Introduction

Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. While *C-myc* is known to drive hepatocarcinogenesis, the roles of its downstream targets remain unclear. NOP56, a conserved nucleolar protein and *C-myc* target, may contribute to HCC progression.

Methods

We analyzed single-cell and bulk transcriptomic datasets to determine NOP56 expression and clinical significance. Loss-of-function assays in HCC cells, along with xenograft models, were used to evaluate its biological role. Protein interaction and pathway analyses were conducted using co-immunoprecipitation and Western blotting.

Results

NOP56 was upregulated in malignant hepatocytes and associated with poor prognosis. NOP56 knockdown inhibited proliferation, colony formation, a

SUBMITTER: Chen H 

PROVIDER: S-EPMC12815711 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature