{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu Z"],"funding":["NCI NIH HHS","National Institutes of Health","NIH HHS","NIGMS NIH HHS"],"pagination":["e2203718"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9875608"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(3)"],"pubmed_abstract":["STING is an innate immune sensor for immune surveillance of viral/bacterial infection and maintenance of an immune-friendly microenvironment to prevent tumorigenesis. However, if and how STING exerts innate immunity-independent function remains elusive. Here, the authors report that STING expression is increased in renal cell carcinoma (RCC) patients and governs tumor growth through non-canonical innate immune signaling involving mitochondrial ROS maintenance and calcium homeostasis. Mitochondrial voltage-dependent anion channel VDAC2 is identified as a new STING binding partner. STING depletion potentiates VDAC2/GRP75-mediated MERC (mitochondria-ER contact) formation to increase mitochondrial ROS/calcium levels, impairs mitochondria function, and suppresses mTORC1/S6K signaling leading to"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["STING Suppresses Mitochondrial VDAC2 to Govern RCC Growth Independent of Innate Immunity."],"pmcid":["PMC9875608"],"funding_grant_id":["R01GM102413","R01 CA243543","R35 GM141833","P30 CA016086","R35GM141833","R01 GM083024","R01 GM102413","R01GM083024"],"pubmed_authors":["Cloer EW","Zhu Z","Zhang J","Liu P","Zhou X","Cook JG","Dotti G","Mei L","Simon JM","Tan X","Major MB","Hepperla AJ","Du H","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"STING Suppresses Mitochondrial VDAC2 to Govern RCC Growth Independent of Innate Immunity.","description":"STING is an innate immune sensor for immune surveillance of viral/bacterial infection and maintenance of an immune-friendly microenvironment to prevent tumorigenesis. However, if and how STING exerts innate immunity-independent function remains elusive. Here, the authors report that STING expression is increased in renal cell carcinoma (RCC) patients and governs tumor growth through non-canonical innate immune signaling involving mitochondrial ROS maintenance and calcium homeostasis. Mitochondrial voltage-dependent anion channel VDAC2 is identified as a new STING binding partner. STING depletion potentiates VDAC2/GRP75-mediated MERC (mitochondria-ER contact) formation to increase mitochondrial ROS/calcium levels, impairs mitochondria function, and suppresses mTORC1/S6K signaling leading to","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2026-05-28T11:32:05.823Z","creation":"2025-04-07T03:19:17.023Z"},"accession":"S-EPMC9875608","cross_references":{"pubmed":["36445063"],"doi":["10.1002/advs.202203718"]}}