ArticleCancer cell international2025
The m6A reader IGF2BP2 promotes pancreatic cancer progression through the m6A-SLC1A5-mTORC1 axis.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- IGF2BP2 remodels the lung metastatic immune microenvironment to promote bladder cancer metastasis.Cellular & molecular immunology · 2026Article
- METTL7A Downregulation Drives SLC1A5-Mediated Glutamine Competition to Promote Tumor Proliferation and Suppress CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- GPSM2 Promotes Pancreatic Cancer Progression Through METTL3-Mediated m6A Modification of YAP1 mRNA.Journal of cellular and molecular medicine · 2026Article
- Interplay of RNA mFASEB bioAdvances · 2026Article
- The RNA methylation modification as an immunometabolic regulatory hub in pancreatic cancer: from mechanistic insights to clinical translation perspectives.Molecular cancer · 2026Review
- SPC25 promotes gastric cancer cells G1/S cell cycle transition and tumorigenesis by enhancing SLC1A5-mediated glutamine metabolism.Journal of bioenergetics and biomembranes · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Mechanisms of mTORC1 and GCN2 amino acid sensing pathways in tumorigenesis and metastatic progression (Review).International journal of molecular medicine · 2026Review
- Post-transcriptional regulation of mRNA stability in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2026Review
- The mMolecular biomedicine · 2025Review
- Epitranscriptomics Regulation of CD70, CD80, and TIGIT in Cancer Immunity.International journal of molecular sciences · 2025Article
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8 authors.
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Abstract
backgroundPancreatic cancer is a highly malignant digestive tumor. Glutamine metabolism is one of the important sources of tumors. N6-methyladenosine (m6A) modification plays a key role in regulating tumor metabolism and holds promise as a therapeutic target in various cancers, including pancreatic cancer. Disrupting m6A regulation of glutamine metabolism could impair tumor growth, offering potential new therapeutic strategies. However, the functional role of m6A modifications in pancreatic cancer, especially in glutamine metabolism, remains poorly understood.
methodsThe Cancer Genome Atlas (TCGA) dataset and GEPIA bioinformatics tool were used to identify the relationship between m6A related proteins and the glutamine metabolism-associated genes, respectively. The biological effects of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) were investigated using in vitro and in vivo models. Methylated RNA immunoprecipitation sequencing (MeRIP-seq), MeRIP-PCR and RNA immunoprecipitation (RIP) were used to identify solute carrier family 1 member 5 (SLC1A5) as a direct target of IGF2BP2.
resultsWe found that IGF2BP2 expression and SLC1A5 were significantly correlated and both highly expressed in pancreatic cancer could predict poor prognosis in patients with pancreatic cancer. Functionally, silencing IGF2BP2 suppressed tumor growth and also inhibited glutamine uptake by tumor cells. Mechanistically, IGF2BP2 induced the m6A-SLC1A5-mTORC1 axis, facilitating the uptake of glutamine by pancreatic cancer cells and accelerate the progress of pancreatic cancer. Furthermore, silencing IGF2BP2 can enhance the sensitivity of pancreatic cancer to radiotherapy and chemotherapy.
conclusionOur findings suggest that IGF2BP2 promotes pancreatic cancer by activating the m6A-SLC1A5 -mTORC1 axis. Targeting the m6A machinery, particularly IGF2BP2, offers a novel therapeutic avenue for pancreatic cancer treatment. By disrupting the regulation of glutamine metabolism, we provide new insights into how m6A-based therapies could enhance the efficacy of current treatments and offer hope for improving patient outcomes in this difficult-to-treat cancer.
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