Answers are grounded in this paper and cite their sources.
Explores ALDH3A2's role in chemoresistance and ferroptosis in acute myeloid leukemia, suggesting enhanced treatment efficacy through inhibition.
Summary Chemoresistance in acute myeloid leukemia (AML) is associated with a poor prognosis in patients. Ferroptosis is one of the mechanisms by which anthracycline exerts anti-leukemic effects, with drug-resistant AML cells exhibiting increased resistance to ferroptosis. Elevated expression of aldehyde dehydrogenase 3 family member A2 (ALDH3A2) is correlated with poor prognosis in patients with AML. Patients with chemo-resistant AML exhibit higher levels of ALDH3A2, particularly the V subtype. ALDH3A2 degraded 4-hydroxynonenal and regulated the fatty acid proportion and content of AML cells, protecting AML cells against doxorubicin-induced ferroptosis. Moreover, overexpression of ALDH3A2 changes cell membrane fluidity and reduces drug uptake. Histone deacetylase 2 binds to the ALDH3A2 promoter and regulates its expression. The inhibition of ALDH3A2 or HDAC enhances chemotherapeutic efficacy in AML.
No takes yet. Share an insight, caveat, or question.
Huang et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: