ArticleCommunications biology2023
Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Novel roles of SETD2 in tumor metabolism and immunotherapy: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Chromatin stability safeguards mitochondrial homeostasis and restrains TORC1 signaling.PLoS genetics · 2026Article
- Antagonistic roles of histone H3 lysine methyltransferases dictate tumor immune surveillance.Nature communications · 2026Article
- Histone Methylation and Chromatin Remodeling in Non-Small Cell Lung Cancer: Mechanisms of Oncogenesis and Emerging Therapeutic Strategies.Biomedicines · 2026Review
- NNMT Loss Drives Cancer Progression by enhancing SAM availability for mTORC1 Signaling and Chromatin Methylation.bioRxiv : the preprint server for biology · 2026Article
- Insights and modulation of RNA polymerase-dependent R-loop and dsRNA in Fanconi anemia hematopoietic stem cells.JCI insight · 2026Article
- Histone methyltransferase SETD2 regulates TKT expression and mediates glycolysis to suppress lung adenocarcinoma progression and improve chemosensitivity.American journal of cancer research · 2026Article
- Characterizing the Clinical and Molecular Profile of SETD2-Mutated Lung Adenocarcinoma.Cancers · 2025Article
- Advances in Computational Drug Repurposing, Driver Genes, and Therapeutics in Lung Adenocarcinoma.Biomolecules · 2025Review
- Identification and validation of an m5C-related lncRNA signature for predicting prognosis and immune response in clear cell renal cell carcinoma.Discover oncology · 2025Article
- The fall of the genome protectors triad: PBRM1, SETD2, and BAP1's impact on metabolism and immunity in clear cell renal cell carcinoma.Frontiers in cell and developmental biology · 2025Review
- Article
- Histone H3 mutations and their impact on genome stability maintenance.Biochemical Society transactions · 2024Review
- Clinical, pathologic and molecular findings in 2 Rottweiler littermates with appendicular osteosarcoma.Research square · 2024Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
SETD2 is a tumor suppressor that is frequently inactivated in several cancer types. The mechanisms through which SETD2 inactivation promotes cancer are unclear, and whether targetable vulnerabilities exist in these tumors is unknown. Here we identify heightened mTORC1-associated gene expression programs and functionally higher levels of oxidative metabolism and protein synthesis as prominent consequences of Setd2 inactivation in KRAS-driven mouse models of lung adenocarcinoma. Blocking oxidative respiration and mTORC1 signaling abrogates the high rates of tumor cell proliferation and tumor growth specifically in SETD2-deficient tumors. Our data nominate SETD2 deficiency as a functional marker of sensitivity to clinically actionable therapeutics targeting oxidative respiration and mTORC1 signaling.
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Registered trials
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.