ENO1 promotes acute myeloid leukemia progression through SCD1-mediated lipid metabolism reprogramming. (PubMed, Blood Adv)
Based on these results, we found that SSI-4, an SCD1 inhibitor, could enhance chemosensitivity of daunorubicin (DNR), which can induce ferroptosis in tumor cells, effectively reduced the resistance to ferroptosis in AML cells exhibiting high ENO1 expression. Overall, our study elucidates the mechanism of ENO1 promotes SCD1 transcription, driving lipid reprogramming and ferroptosis resistance within AML. Additionally, it highlights the therapeutic potential of combining SCD1 inhibition with DNR for AML patients with elevated ENO1 expression levels.