ArticleCancer gene therapy2026
PRDX1 depletion predisposes to ferroptosis through inhibiting the cAMP pathway in B-cell acute lymphoblastic leukemia.
Article in Cancer gene therapy, 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
B-cell acute lymphoblastic leukemia (B-ALL) is a hematologic malignancy commonly found in pediatric patients. This study aims to screen hub genes in B-ALL and elucidate the role of peroxiredoxin 1 (PRDX1) in the modulation of ferroptosis. Bioinformatics analyses were conducted to identify pivotal genes in the GSE17703 and GSE48558 datasets. The biological effects of PRDX1 deletion in B-ALL cells and the xenograft tumor were evaluated using a series of functional assays. Ferroptosis was induced in B-ALL cells using erastin. Transcriptome sequencing was performed on Nalm-6 cells before and after PRDX1 knockdown. Forskolin was employed to explore the role of PRDX1 in the cyclic adenosine monophosphate (cAMP) pathway. Four pivotal genes were identified, with two genes upregulated and two downregulated. Depletion of PRDX1 suppressed the proliferative, migratory, and invasive abilities of B-ALL cells, whereas PRDX1 overexpression exerted the opposite effects. PRDX1 silencing promoted erastin-induced ferroptosis, including elevated levels of COX2, ACSL4, ferrous ions, ROS, and MDA, while reducing GPX4, GSH, and SOD levels. PRDX1 knockdown further reduced the viability of B-ALL cells treated with the ferroptosis activator ML210, and treatment with the ferroptosis inhibitor liproxstatin-1 significantly reversed the suppressive effect of PRDX1 knockdown on xenograft tumor growth. Mechanically, PRDX1 deletion triggered ferroptosis in B-ALL cells by inhibiting the cAMP pathway. PRDX1 deficiency modulates ferroptosis in B-ALL cells by blocking the cAMP pathway, which offer a novel perspective on the pathogenesis of B-ALL.
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