ArticleBlood2025
PSTK inhibition activates cGAS-STING, precipitating ferroptotic cell death in leukemic stem cells.
Article in Blood, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities.Cell death discovery · 2026Review
- Selenoproteins: Minute yet vital players governing cellular fate.Genes & diseases · 2026Review
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- Zalcitabine induces ferroptosis in multiple myeloma through the TFAM-cGAS-STING-SLC7A11 axis.Journal of translational medicine · 2026Article
- Research advances in single-molecule multi-target strategies targeting ferroptosis for colorectal cancer treatment.American journal of cancer research · 2026Review
- USP11-PGAM5 Axis Promotes Neurotoxic Astrocyte Reactivity by Aggravating the mtDNA-cGAS-STING Pathway After Intracerebral Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Redox-Amino Acid Metabolic Crosstalk in Ovarian Cancer Stem Cells: Integrating Metabolic Reprogramming, Signaling, and the Tumor Microenvironment.Antioxidants (Basel, Switzerland) · 2025Review
- The prognostic marker NRIP1 is associated with tumor progression and immune infiltration in acute myeloid leukemia.Acta biochimica et biophysica Sinica · 2025Article
- Breaking barriers: The cGAS-STING pathway as a novel frontier in cancer immunotherapy.Cancer communications (London, England) · 2025Review
- Review
- Targeting the interplay of cGAS-STING and ferroptosis by nanomedicine in the treatment of cancer.Journal of experimental & clinical cancer research : CR · 2025Review
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Authors and funding
21 authors.
Funding
Abstract
abstractDifferentiation arrest and dependence on oxidative metabolism are features shared among genetically diverse acute myeloid leukemias (AMLs). A phenotypic CRISPR-CRISPR-associated protein 9 screen in AML identified dependence on phosphoseryl-transfer RNA kinase (PSTK), an atypical kinase required for the biosynthesis of all selenoproteins. In vivo, PSTK inhibition (PSTKi) impaired AML cell growth and leukemic stem cell self-renewal. Notably, timed pharmacologic PSTKi effectively targeted chemotherapy-resistant AML in murine and patient-derived xenograft models, showing selectivity for malignant cells over normal hematopoietic cells. Mechanistically, PSTKi-induced reactive oxygen species (ROS) triggering mitochondrial DNA release into the cytosol and activated cyclic GMP-AMP Synthase-Stimulator of interferon genes (cGAS-STING). This activation, in turn, disrupted iron metabolism, augmenting ROS generation, and amplifying ferroptosis. Together, these findings reveal a self-reinforcing PSTK-cGAS-STING-ROS loop, culminating in an oxidative crisis and ferroptotic cell death of leukemic stem cells. These data highlight the potential for augmenting standard cancer chemotherapies using timed metabolic intervention to eliminate chemotherapy-persisting cells and thereby impede disease relapse.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.