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September 10, 2025HaematologicaOpen Access

SLC25A1 reprograms mitochondrial and fatty acid metabolism to promote the progression of acute myeloid leukemia

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Authors

MCMiao ChenWLWenze LiTYTao Yuan

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Overview

Analysis reveals SLC25A1's crucial function in AML progression and lipid metabolism, suggesting therapeutic potential.

Key Points

  • SLC25A1 inhibition significantly reduces AML cell proliferation and induces apoptosis.
  • Elevated SLC25A1 expression correlates with poor prognosis in AML patients.
  • Inhibiting SLC25A1 disrupts citrate homeostasis, causing mitochondrial dysfunction.
  • CTPI3, a novel SLC25A1 inhibitor, powerfully suppresses AML progression and enhances drug efficacy.

Cite This Study

Chen et al. (2025) studied this question.

synapsesocial.com/papers/68c23bd7b210217d6478701dhttps://doi.org/10.3324/haematol.2024.287269
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Also Consider

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  1. 1SLC44A1 promotes AML progression and chemoresistance by regulating the Notch signaling pathway2026
  2. 2Inhibition of CPT1A reverses AML1-ETO-induced differentiation blockage by activating BCL-2/MYC signaling and metabolic reprogramming2025
  3. 3Tumor intrinsic regulation of PD-L1 and of interferon Type I via an SLC25A1-driven mitochondrial pathway, influences the anti-tumor immune response2025 · 1 citations
  4. 4SLC25A39 overexpression exacerbates lung adenocarcinoma progression and is negatively regulated by AFG3L22025 · 1 citations
  5. 562The SLC1A1/EAAT3 dicarboxylic amino acid transporter is an epigenetically dysregulated nutrient carrier that sustains oncogenic metabolic programs2025