ArticleMaterials today. Bio2026
CXCR4 antagonistic lipid nanoparticles loading siRNA combat refractory AML through AML1-ETO depletion and homoharringtonine sensitization.
Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute myeloid leukemia (AML) is characterized by uncontrolled malignant clonal proliferation of leukemic cells resulting from the blockade of myeloid hematopoietic stem/progenitor cell differentiation. The disease-causing fusion protein AML1-ETO (also known as RUNX1-ETO or RUNX1-RUNX1T1) and the chemokine (C-X-C motif) receptor 4 (CXCR4) have been recognized as crucial effectors. Strategies targeting each individual factor have been applied to develop new therapeutic approaches; however, clinical demands remain unmet, and much is still unknown about the crosstalk between the two factors. In this study, we utilized a lipid nanoparticle platform to carry AML1-ETO siRNA and the CXCR4 antagonistic peptide E5 (E5-LNP@siAE) to simultaneously deplete the fusion protein and inhibit CXCR4 activation, aiming to elucidate the crosstalk between the two factors and to develop a novel dual-functional therapeutic approach based on lipid nanoparticles. The resulting nanoparticles were investigated in a refractory AML mouse model (AML1-ETO & C-KIT
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