ArticleCancer & metabolism2025
ETV4/ALYREF-mediated glycolytic metabolism through PKM2 enhances resistance to ferroptosis and promotes the development of intrahepatic cholangiocarcinoma.
Article in Cancer & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- mBiology direct · 2026Review
- RNA modifications and cancer ferroptosis.Cancer cell international · 2026Review
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- ALYREF regulates glycolysis and promotes the progression of endometrial cancer through mFrontiers in cell and developmental biology · 2026Article
- Hypoxia Triggers ALYREF-Mediated mThe Kaohsiung journal of medical sciences · 2026Article
- Characterization of Differential GPX4 Essentiality Between Intrahepatic and Extrahepatic Cholangiocarcinoma via Leveraging of a Large-Scale Functional Genomic Screen.International journal of molecular sciences · 2025Article
- Epitranscriptomic mechanisms and implications of RNA mTheranostics · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundIntrahepatic cholangiocarcinoma (ICC) is the second most common primary hepatocellular cancer. This study investigated whether ETV4, ALYREF, and PKM2 affect glycolytic metabolism and ferroptosis, thereby potentially influencing ICC.
methodsBioinformatic analysis was used to explore the expression levels and prognosis of ETV4, ALYREF, and PKM2 in ICC and their regulatory relationships were confirmed using in vitro experiments. Glycolytic metabolism and ferroptosis were examined, and chromatin immunoprecipitation and RNA immunoprecipitation experiments were performed to verify whether the ETV4, PKM2, and ALYREF could bind. The effect of ETV4/ALYREF on ICC was further confirmed by in vivo experiments.
resultsETV4, ALYREF, and PKM2 were highly expressed in ICC. Overexpressed (oe)-ETV4 and oe-PKM2 promoted cell migration and increased glucose (GLU) utilization and lactate and intracellular adenosine triphosphate (ATP) production. Addition of the ferroptosis inducer Erastin to the above groups revealed that sh-ETV4 and sh-ALYREF increased lipid reactive oxygen species (ROS), malondialdehyde (MDA), and Fe
conclusionETV4 promotes ICC development and ferroptosis resistance by facilitating glycolytic metabolism, and regulating PKM2 transcription by directly binding to the PKM2 promoter. Additionally, it mediates m5C-dependent PKM2 stabilization by directly binding to ALYREF. This study identified a new potential therapeutic target for ICC.
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