ArticleLeukemia2024
STING is crucial for the survival of RUNX1::RUNX1T1 leukemia cells.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities.Cell death discovery · 2026Review
- WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.Nature communications · 2026Article
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- Review
- Genome-Wide Detection of Leukemia Biomarkers from lincRNA-Protein-Coding Gene Interaction Networks in the Three-Dimensional Chromatin Structure.Current issues in molecular biology · 2025Article
- Identification and validation of three tumor suppressors associated with the immune response of acute myeloid leukemia.Frontiers in genetics · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Even though acute myeloid leukemia (AML) patients with a RUNX1::RUNX1T1 (AE) fusion have a relatively favorable prognosis, approximately 50% relapse within 2.5 years and develop resistance to subsequent chemotherapy [1]. It is therefore imperative to identify novel therapeutic targets for AE leukemia to improve outcomes. In this study, we unveil that targeting STING effectively suppresses the growth of AE leukemia cells. Both genetic and pharmacological inhibition of STING lead to the diminish of AE leukemia cells. Importantly, in a mouse primary AE leukemia model, STING deletion significantly attenuates leukemogenesis and prolongs the animals' lifespan. Blocking the downstream inflammatory pathway of STING yields similar effects to STING inhibition in AE leukemia cells, highlighting the pivotal role of STING-dependent inflammatory responses in sustaining the survival of AE leukemia cells. Moreover, through a genome-wide CRISPR screen, we identified fatty acid desaturase 2 (FADS2) as a non-canonical factor downstream of STING inhibition that mediates cell death. Inhibition of STING releases FADS2 activity, consequently inducing the synthesis of polyunsaturated fatty acids (PUFAs) and triggering lipid peroxidation-associated cell death [2]. Taken together, these findings reveal a critical function of STING in the survival of AE-positive AML cells and suggest STING to be a potential therapeutic target for clinical intervention in these patients.
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