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December 8, 2025BloodOpen Access

FGF11–HIF-1α glycolytic epigenetic axis drives AML progression and chemoresistance via metabolic reprogramming

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Authors

HLHang LvXZXin ZhuangXMXiaoying Man

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Overview

Functional assays reveal metabolic reprogramming drives drug resistance in AML, highlighting the role of FGF11 and HIF-1α.

Key Points

  • This research aims to identify the role of the FGF11-HIF-1α axis in acute myeloid leukemia progression and chemoresistance.
  • Analyses of FGF11 and HIF-1α expression in 173 AML patient samples and 2 cell lines using RNA-seq and qPCR.
  • Functional studies employed siRNA knockdown and rhFGF11 supplementation.
  • Metabolic flux analysis measured glycolysis and oxidative phosphorylation rates.
  • FGF11 mRNA was 4.3-fold higher in AML blasts than in normal bone marrow, predicting shorter event-free survival.
  • FGF11 repression of oxidative metabolism was demonstrated by down-regulation of HIF-1α signaling after knockdown.
  • Exogenous rhFGF11 enhanced migration and triggered a metabolic shift from oxidative phosphorylation to glycolysis.

Cite This Study

Lv et al. (2025) studied this question.

synapsesocial.com/papers/69362f4e4fa91c937236d82chttps://doi.org/10.1182/blood-2025-3185
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Also Consider

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  5. 5Abstract 5967: Overexpression of the transcription factor gene TGIF1 inhibits proliferation in NRAS-driven acute myeloid leukemia cells2026