ArticleRedox biology2025
FTO facilitates colorectal cancer chemoresistance via regulation of NUPR1-dependent iron homeostasis.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- METTL3-mediated m⁶A methylation of E2F2 targets MCU to promote the malignant phenotype of gastric cancer cells.Cancer gene therapy · 2026Article
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- Fat Mass and Obesity-Associated Protein Contributes to Tumorigenesis and Drug Resistance of Diffuse Large B-Cell Lymphoma by Suppressing N6-Methyladenosine Methylation of Myc.The Kaohsiung journal of medical sciences · 2026Article
- NUPR1 as a central stress-adaptation node in cancer: integrating metabolic rewiring, cell death, and therapy resistance.Journal of biomedical science · 2026Review
- Lipocalin 2: a double-edged sword in cellular ferroptosis.Cell biology and toxicology · 2026Review
- FTO-Mediated m6A Demethylation of SERPINF1 Attenuates Multiple Myeloma Progression via the Wnt/β-Catenin Pathway.Journal of microbiology and biotechnology · 2026Article
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- Targeting of the mNature communications · 2025Article
- ALKBH5-mediated NPC2 mRNA mFunctional & integrative genomics · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance in colorectal cancer (CRC) poses a major challenge for cancer therapy and stands as the primary cause of cancer-related mortality. The N6-methyladenosine (m6A) modification has emerged as a pivotal regulator in cancer biology, yet the precise m6A regulators that propel CRC progression and chemoresistance remain elusive. Our study established a significant correlation between m6A regulatory gene expression profiles and CRC severity. Notably, based on the knockout cellular and mouse model created by CRISPR/Cas9-mediated genome engineering, we identified m6A demethylase FTO emerged as a pivotal orchestrator of CRC chemoresistance through the regulation of NUPR1, a critical transcription factor involved in iron homeostasis via LCN2 and FTH1. Mechanistic study revealed that FTO stabilized NUPR1 mRNA by specifically targeting the +451 m6A site, thereby preventing YTHDF2-mediated degradation of NUPR1 mRNA. Moreover, the simultaneous targeting of FTO and NUPR1 dramatically enhanced the efficacy of chemotherapy in CRC cells. Our findings underscore the potential of modulating the m6A methylome to overcome chemoresistance and highlight the FTO-NUPR1 axis as a critical determinant in CRC pathobiology.
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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.