ArticleCytotechnology2023
The m6A reader IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties, and immune resistance of non-small-cell lung cancer stem cells.
Article in Cytotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Systematic analysis of IGF2BP family members in non-small-cell lung cancer.Human genomics · 2024Pooled it
- Effects of Tumor Microenvironment on Lung Cancer Stem Cells: Bidirectional Regulatory Mechanisms.Cancer medicine · 2026Review
- Differences in the expression profiles of m6A-related genes and the prognostic role in immunotherapy for lung adenocarcinoma patients.Frontiers in oncology · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- Prognostic role and mutational characteristics of N6-methyladenosine-related genes in lung adenocarcinoma.Oncology letters · 2025Article
- The mMolecular biomedicine · 2025Review
- The biological roles and molecular mechanisms of m6A reader IGF2BP1 in the hallmarks of cancer.Genes & diseases · 2025Review
- EFTUD2 is a promising diagnostic and prognostic indicator involved in the tumor immune microenvironment and glycolysis of lung adenocarcinoma.Frontiers in oncology · 2025Article
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in hematological diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) modification is the most common internal modification in eukaryotic mRNA and an important mechanism for post-transcriptional regulation of genes. This study focuses on the role of the m6A reader insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) in the malignant behaviors of non-small-cell lung cancer (NSCLC) cells and especially the cancer stem cells (CSCs). We obtained IGF2BP1 as an aberrantly upregulated gene linking to poor survival of patients with NSCLC by bioinformatics, and then confirmed increased IGF2BP1 expression in NSCLC tissues and cells, especially in the enriched CSCs. Knockdown of IGF2BP1 suppressed proliferation, mobility and epithelial-mesenchymal transition activity of NSCLC cells and CSCs, and it reduced stemness, self-renewal ability, xenograft tumorigenesis and immune resistance of the CSCs. IGF2BP1 was predicted to have a positive correlation with BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B), and it upregulated BUB1B expression through m6A modification. Further overexpression of BUB1B in CSCs counteracted the effects of IGF2BP1 silencing and restored the malignant phenotype, self-renewal, and immune resistance of CSCs in vitro and in vivo. Taken together, this work demonstrates that IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties and immune resistance of NSCLC stem cells.
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