ArticleCell death & disease2015
IMP2/p62 induces genomic instability and an aggressive hepatocellular carcinoma phenotype.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 92 citations in OpenAlex.
- Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- The insulin-like growth factor 2 mRNA-binding protein 2 affects tumor cell metabolism via mitochondrial transporter activity and lipid alterations.Cell death discovery · 2026Article
- HyperTRIBE identifies hepatic IGF2BP2/IMP2 targetsNAR molecular medicine · 2026Article
- Th17 cells favor migration and invasiveness of cervical cancer cells under hypoxia in an IGF2BP2-dependent manner.International journal of cancer · 2026Article
- NMolecular medicine reports · 2026Article
- Function and regulatory mechanism of RNA-binding protein IGF2BP2 in obesity and cancers.Molecular biology reports · 2026Review
- Article
- Review of roles of RNA-binding proteins on NAFLD and the related pharmaceutical measures.Biomolecules & biomedicine · 2025Review
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- Bioinformatic identification reveals a m6A-binding protein, IGF2BP2, as a novel tumor-promoting gene signature in thyroid carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- The RNA binding protein IGF2BP2/IMP2 alters the cargo of cancer cell-derived extracellular vesicles supporting tumor-associated macrophages.Cell communication and signaling : CCS · 2024Article
- Insulin-like growth factor 2 mRNA-binding protein 2 is a therapeutic target in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- A combined computational and functional approach identifies IGF2BP2 as a driver of chemoresistance in a wide array of pre-clinical models of colorectal cancer.Molecular cancer · 2023Article
- RNA N6-methyladenosine modification in regulating cancer stem cells and tumor immune microenvironment and its implication for cancer therapy.Journal of cancer research and clinical oncology · 2023Review
- IGF2BP2 promotes head and neck squamous carcinoma cell proliferation and growth via the miR-98-5p/PI3K/Akt signaling pathway.Frontiers in oncology · 2023Article
- IGF2BP2 promotes cancer progression by degrading the RNA transcript encoding a v-ATPase subunit.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Comment on: The m6A Reader IGF2BP2 Regulates Macrophage Phenotypic Activation and Inflammatory Diseases by Stabilizing TSC1 and PPARγ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- RNA N6-methyladenosine reader IGF2BP2 promotes lymphatic metastasis and epithelial-mesenchymal transition of head and neck squamous carcinoma cells via stabilizing slug mRNA in an m6A-dependent manner.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related deaths and commonly develops in inflammatory environments. The IGF2 mRNA-binding protein IMP2-2/IGF2BP2-2/p62 was originally identified as an autoantigen in HCC. Aim of this study was to investigate a potential pathophysiological role of p62 in hepatocarcinogenesis. Human HCC tissue showed overexpression of IMP2, which strongly correlated with the fetal markers AFP and DLK1/Pref-1/FA-1 and was particularly elevated in tumors with stem-like features and hypervascularization. Molecular classification of IMP2-overexpressing tumors revealed an aggressive phenotype. Livers of mice overexpressing the IMP2 splice variant p62 highly expressed the stem cell marker DLK1 and secreted DLK1 into the blood. p62 was oncogenic: diethylnitrosamine (DEN)-treated p62 transgenic mice exhibited a higher tumor incidence and multiplicity than wild types. Tumors of transgenics showed a more aggressive and stem-like phenotype and displayed more oncogenic chromosomal aberrations determined with aCGH analysis. DEN-treated p62 transgenic mice exhibited distinct signs of inflammation, such as inflammatory cytokine expression and oxidative stress markers, that is, thiobarbituric acid-reactive substance (TBARS) levels. Reactive oxygen species (ROS) production was elevated in HepG2 cells, which either overexpressed p62 or were treated with DLK1. p62 induced this ROS production by a DLK1-dependent induction and activation of the small Rho-GTPase RAC1, activating NADPH oxidase and being overexpressed in human HCC. Our data indicate that p62/IMP2 promotes hepatocarcinogenesis by an amplification of inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.