ArticleNature communications2024
Cholesterol-binding motifs in STING that control endoplasmic reticulum retention mediate anti-tumoral activity of cholesterol-lowering compounds.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 52 citations in OpenAlex.
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- Atlas-ing STING mutations to advance fundamental understanding and clinical translation.Cell research · 2026Article
- Evolutionary conservation analysis reveals a primordial function of STING as a regulator of lipid metabolism via FADS2.Nature communications · 2026Article
- The cGAS/STING pathway in cancer: translating innate DNA sensing into therapeutic potential.The Journal of clinical investigation · 2026Review
- STING signalling as a mediator between lipid metabolism and innate immunity.Nature reviews. Molecular cell biology · 2026Article
- Detection of nuclear STING in cultured human cells and in the normal and cancer tissues.iScience · 2026Article
- Apolipoproteins L involvement in immunity.Journal of human immunity · 2026Review
- Article
- Recycling senescent cell lipids for targeted senotherapy.Nature communications · 2026Article
- Ginsenoside Rb1 Targets the HRD1-STING Axis to Mitigate Cholesterol-Induced VSMC Senescence.Journal of clinical laboratory analysis · 2026Article
- Opportunities and challenges of targeting cGAS-STING in cancer.Nature reviews. Cancer · 2026Review
- Sino-C, a novel sinomenine derivative, induces cell death by disrupting cholesterol homeostasis in colorectal cancer cells.Acta pharmacologica Sinica · 2026Article
- Lifelong cGAS deficiency leads to altered lipid storage and cholesterol homeostasis.Biological research · 2026Article
- Targeted Lipid Metabolism Screening Uncovers Regulatory Effects on the STING Immune Response in Mevalonate, Eicosanoid and Fatty Acid Pathways.bioRxiv : the preprint server for biology · 2026Article
- Targeted lipid metabolism screening uncovers regulatory effects on the STING immune response in mevalonate, eicosanoid and fatty acid pathways.Frontiers in immunology · 2026Article
- Regulation of STING activation by phosphoinositide and cholesterol.bioRxiv : the preprint server for biology · 2025Article
- Cascade-targeted delivery platform enhances antigen cross-presentation and STING activation for durable cellular immunity.Bioactive materials · 2025Article
- Host-related Determinants of Response to Immunotherapy in Non-small Cell Lung Cancer: The Interplay of Body Composition, Metabolism, Sex and Immune Regulation.Current oncology reports · 2025Review
- Silencing PCSK9 reshapes the spatiotemporal activation of STING for safe and effective cancer immunotherapy.Nature communications · 2025Article
- Mitochondria relay cholesterol signal exacerbates osteoarthritis in mice.Nature communications · 2025Article
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
Abstract
The cGAS-STING pathway plays a crucial role in anti-tumoral responses by activating inflammation and reprogramming the tumour microenvironment. Upon activation, STING traffics from the endoplasmic reticulum (ER) to Golgi, allowing signalling complex assembly and induction of interferon and inflammatory cytokines. Here we report that cGAMP stimulation leads to a transient decline in ER cholesterol levels, mediated by Sterol O-Acyltransferase 1-dependent cholesterol esterification. This facilitates ER membrane curvature and STING trafficking to Golgi. Notably, we identify two cholesterol-binding motifs in STING and confirm their contribution to ER-retention of STING. Consequently, depletion of intracellular cholesterol levels enhances STING pathway activation upon cGAMP stimulation. In a preclinical tumour model, intratumorally administered cholesterol depletion therapy potentiated STING-dependent anti-tumoral responses, which, in combination with anti-PD-1 antibodies, promoted tumour remission. Collectively, we demonstrate that ER cholesterol sets a threshold for STING signalling through cholesterol-binding motifs in STING and we propose that this could be exploited for cancer immunotherapy.
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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.