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Highlights • GILT is upregulated in chemoresistant LSC-enriched CD34+ progenitor cells.• Inhibition of GILT in AML cells sensitized them to Ara-C treatment through ROS-mediated mitochondrial damage and apoptosis.• PI3K/Akt/NRF2 pathway… Click to show full abstract
Highlights • GILT is upregulated in chemoresistant LSC-enriched CD34+ progenitor cells.• Inhibition of GILT in AML cells sensitized them to Ara-C treatment through ROS-mediated mitochondrial damage and apoptosis.• PI3K/Akt/NRF2 pathway inhibition is critical for the intracellular oxidative state in GILT-suppression AML cells after Ara-C treatment.• GILT expression is related to a poor prognosis in AML patients.
Keywords:
mitochondrial damage;
mediated mitochondrial;
ros mediated;
targeting ifn;
aml
Journal Title: Translational Oncology
Year Published: 2021
Link to full text (if available)
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Journal Title: Translational Oncology
Year Published: 2021
Link to full text (if available)
Share on Social Media: Sign Up to like & get
recommendations!