The m6A reader IGF2BP3 promotes HCC progression by enhancing MCM10 stability
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View abstract on PubMed
Summary
This summary is machine-generated.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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