ArticleNature cancer2026
PAPOLA-mediated hyperactive polyadenylation promotes leukemogenesis and leukemia stem cell self-renewal through metabolic reprogramming.
Article in Nature cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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Who cites it
1 citing paper in PubMed.
- A polyadenylation enzyme rewires metabolism to fuel AML.Nature cancer · 2026Article
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19 authors.
Funding
Abstract
Polyadenylation is essential for mRNA stability and translational efficiency. Although poly(A) tail length is dynamically regulated under physiological conditions, its dysregulation and functional importance in cancer remain poorly understood. Here, we identify widespread poly(A) tail elongation and aberrant upregulation of poly(A) polymerase alpha (PAPOLA) in acute myeloid leukemia (AML), with high PAPOLA expression associated with poor clinical outcomes. Using primary AML samples, leukemia cell lines and multiple mouse models, we demonstrate that PAPOLA-driven hyperactive polyadenylation promotes leukemogenesis and sustains leukemia stem cell maintenance. Mechanistically, PAPOLA enhances metabolic reprogramming by upregulating glutathione S-transferase mu 2 (GSTM2), which activates the 4-hydroxynonenal (HNE)-dihydrolipoamide dehydrogenase (DLD) axis to drive AML progression. Notably, pharmacological inhibition of PAPOLA with cordycepin suppresses metabolic reprogramming and impairs leukemogenesis. Overall, our findings establish hyperactive polyadenylation as a core oncogenic mechanism linking RNA processing to cancer metabolism in AML, highlighting the PAPOLA-GSTM2-HNE-DLD axis as a promising therapeutic target.
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