Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 10, 2025HaematologicaOpen Access

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

View Full Paper
Ask AI
Bookmark
Share

Authors

MCMiao ChenSun Yat-sen UniversityWLWenze LiInner Mongolia Agricultural UniversityTYTao YuanUniversity of Electronic Science and Technology of China

Discussion

Loading...

Member takes

Implication

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/68c18c019b7b07f3a0614715https://doi.org/10.3324/haematol.2024.287269
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1SLC44A1 promotes AML progression and chemoresistance by regulating the Notch signaling pathway2026
  2. 2SLC25A21 correlates with the prognosis of adult acute myeloid leukemia through inhibiting the growth of leukemia cells via downregulating CXCL82024 · 5 citations
  3. 3CPT1B promotes acute myeloid leukemia progression via fatty acid oxidation–dependent metabolic reprogramming2026
  4. 4SLC25A20 promotes tumor growth by reprogramming energy metabolism in lung adenocarcinoma2026
  5. 5Inhibition of CPT1A reverses AML1-ETO-induced differentiation blockage by activating BCL-2/MYC signaling and metabolic reprogramming2025