Nitidine chloride inhibits the progression of hepatocellular carcinoma by suppressing IGF2BP3 and modulates metabolic pathways in an m⁶A-dependent manner.

ABSTRACT:

Background

Hepatocellular carcinoma (HCC) stands as a major health concern due to its significant morbidity and mortality. Among potential botanical therapeutics, nitidine chloride (NC) has garnered attention for its potential anti-HCC properties. However, the underlying mechanisms, especially the possible involvement of the m⁶A pathway, remain to be elucidated.

Methods

HCC cell and zebrafish xenograft models were utilized to validate the anti-HCC effects of NC. RNA-seq and MeRIP-seq analyses were performed to explore the potential targets and mechanisms of NC against HCC. The target effect of NC on IGF2BP3 was verified through RT-qPCR, WB, molecular docking, molecular dynamics (MD) simulation, surface plasmon resonance (SPR), and CCK8 off-target assays. Downstrea

SUBMITTER: Xiong DD 

PROVIDER: S-EPMC11796242 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature