{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Y"],"funding":["NIBIB NIH HHS","NIAID NIH HHS","NCI NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","U.S. Department of Health &amp; Human Services | National Institutes of Health"],"pagination":["856-866"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11948844"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(6)"],"pubmed_abstract":["The efficacy of STING (stimulator of interferon genes) agonists is due to various factors, primarily inefficient intracellular delivery, low/lack of endogenous STING expression in many tumours, and a complex balance between tumour control and progression. Here we report a universal STING mimic (uniSTING) based on a polymeric architecture. UniSTING activates STING signalling in a range of mouse and human cell types, independent of endogenous STING expression, and selectively stimulates tumour control IRF3/IFN-I pathways, but not tumour progression NF-κB pathways. Intratumoural or systemic injection of uniSTING-mRNA via lipid nanoparticles (LNPs) results in potent antitumour efficacy across established and advanced metastatic tumour models, including triple-negative breast cancer, lung cance"],"journal":["Nature nanotechnology"],"pubmed_title":["Universal STING mimic boosts antitumour immunity via preferential activation of tumour control signalling pathways."],"pmcid":["PMC11948844"],"funding_grant_id":["R01 EB032865","R01EB032865","R35 CA232109","R01-AI029564","R01 AI029564","T32 CA196589","R35-CA232109"],"pubmed_authors":["McCabe E","Yang Y","Li S","Hu M","Withrow AM","Liu R","Zhang L","Wang Y","Ting JP"],"additional_accession":[]},"is_claimable":false,"name":"Universal STING mimic boosts antitumour immunity via preferential activation of tumour control signalling pathways.","description":"The efficacy of STING (stimulator of interferon genes) agonists is due to various factors, primarily inefficient intracellular delivery, low/lack of endogenous STING expression in many tumours, and a complex balance between tumour control and progression. Here we report a universal STING mimic (uniSTING) based on a polymeric architecture. UniSTING activates STING signalling in a range of mouse and human cell types, independent of endogenous STING expression, and selectively stimulates tumour control IRF3/IFN-I pathways, but not tumour progression NF-κB pathways. Intratumoural or systemic injection of uniSTING-mRNA via lipid nanoparticles (LNPs) results in potent antitumour efficacy across established and advanced metastatic tumour models, including triple-negative breast cancer, lung cance","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2025-06-28T03:05:23.86Z","creation":"2025-06-28T03:05:23.86Z"},"accession":"S-EPMC11948844","cross_references":{"pubmed":["38480836"],"doi":["10.1038/s41565-024-01624-2"]}}