Nature Cancer：中山大学林水宾/赵萌/包勇合作揭示多聚腺苷酸化酶促进白血病的新机制，而虫草素可抑制这一过程
Merged summary
TL;DR - A Nature Cancer study identifies PAPOLA-driven excessive mRNA polyadenylation as a mechanism promoting acute myeloid leukemia (AML). Pharmacological PAPOLA inhibition with cordycepin suppressed metabolic reprogramming and weakened leukemogenesis in experimental models.
- AML samples showed elongated poly(A) tails and elevated PAPOLA, with high PAPOLA expression associated with poor prognosis.
- PAPOLA promoted leukemia and leukemia stem-cell self-renewal across primary samples, cell lines, and mouse models.
- The mechanism involves GSTM2 upregulation and activation of the HNE–DLD metabolic signaling axis.
- The PAPOLA–GSTM2–HNE–DLD axis represents a potential therapeutic target, though the reported evidence is preclinical.
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Nature Cancer：中山大学林水宾/赵萌/包勇合作揭示多聚腺苷酸化酶促进白血病的新机制，而虫草素可抑制这一过程
TL;DR - A Nature Cancer study identifies PAPOLA-driven excessive mRNA polyadenylation as a mechanism promoting acute myeloid leukemia (AML). Pharmacological PAPOLA inhibition with cordycepin suppressed metabolic reprogramming and weakened leukemogenesis in experimental models.
- AML samples showed elongated poly(A) tails and elevated PAPOLA, with high PAPOLA expression associated with poor prognosis.
- PAPOLA promoted leukemia and leukemia stem-cell self-renewal across primary samples, cell lines, and mouse models.
- The mechanism involves GSTM2 upregulation and activation of the HNE–DLD metabolic signaling axis.
- The PAPOLA–GSTM2–HNE–DLD axis represents a potential therapeutic target, though the reported evidence is preclinical.