ArticleArchives of medical science : AMS2026
UBC9 silencing-mediated PPARα deSUMOylation induces inhibition of cell proliferation by ferroptosis in acute myeloid leukemia.
Article in Archives of medical science : AMS, 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
Introduction: Inhibited acute myeloid leukemia (AML) proliferation is accompanied by downregulated peroxisome proliferator-activated receptor α (PPARα), which however can be stabilized via SUMOylation. This study investigated how PPARα SUMOylation impacts AML cell growth. Material and methods: Human AML HL-60 and Tohoku Hospital Pediatrics-1 (THP-1) cells were treated with the PPARα inhibitor GW6471 (10 µM) for 24 and 48 h. THP-1 cells were exposed to the PPARα agonist pirinixic acid (10 µM) following manipulation of the expression of the small ubiquitin-like modifier protein (SUMO)-conjugating enzyme UBC9. The interaction between PPARα and SUMO1 was detected by immunoprecipitation assay. HL-60 and THP-1 cell viability, apoptosis, and ferroptosis were measured via Cell Counting Kit-8 assay, flow cytometry, BODIPY-C11 staining and/or colorimetric assay. UBC9, glutathione peroxidase 4 (GPX4), recombinant solute carrier family 7, member 11(SLC7A11) and PPARα expression levels were analyzed by qRT-PCR or Western blot. Results: GW6471 treatment for 24 and 48 h suppressed viability, promoted apoptosis and lipid peroxidation, increased the level of Fe Conclusions: UBC9 silencing-induced PPARα deSUMOylation induces suppression of AML cell growth by ferroptosis.
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