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Updated: May 23, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
The m6A reader IGF2BP3 promotes HCC progression by enhancing MCM10 stability
Lianwu Zhao1, Hongyan Huang1, Linfei Luo1
1Department of Gastroenterology, The 2nd Affiliated Hospital, Jiangxi Medical College, Nanchang University, Jiangxi, 330000, People's Republic of China.
Abnormal N6-methyladenosine (m6A) modifications are linked to cancer. Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) promotes liver cancer progression by stabilizing m6A-modified RNA, indicating its potential as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Aberrant N6-methyladenosine (m6A) modifications are implicated in cancer progression.
- The specific roles of m6A regulators in cancer, particularly liver hepatocellular carcinoma (HCC), require further elucidation.
Purpose of the Study:
- To investigate the function and mechanism of insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) in liver hepatocellular carcinoma (HCC).
- To determine if IGF2BP3 acts as an m6A regulator in HCC tumorigenesis.
Main Methods:
- Quantitative analysis of IGF2BP3 expression in HCC tissues.
- In vitro and in vivo experiments involving IGF2BP3 silencing in HCC cells.
- RNA immunoprecipitation assays to identify IGF2BP3-interacting RNAs.
Main Results:
- IGF2BP3 is overexpressed in HCC and correlates with poor prognosis.
- IGF2BP3 silencing inhibits HCC cell proliferation and migration in vitro and in vivo.
- IGF2BP3 binds to minichromosomal maintenance complex component (MCM10) mRNAs, stabilizing m6A-modified RNA.
Conclusions:
- IGF2BP3 acts as an oncogene in HCC by promoting tumorigenesis in an m6A-dependent manner.
- IGF2BP3 is a potential prognostic biomarker and therapeutic target for HCC.
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