{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rufo N"],"funding":["Austrian Science Fund FWF"],"pagination":["230-245"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8738768"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(1)"],"pubmed_abstract":["Mounting evidence indicates that immunogenic therapies engaging the unfolded protein response (UPR) following endoplasmic reticulum (ER) stress favor proficient cancer cell-immune interactions, by stimulating the release of immunomodulatory/proinflammatory factors by stressed or dying cancer cells. UPR-driven transcription of proinflammatory cytokines/chemokines exert beneficial or detrimental effects on tumor growth and antitumor immunity, but the cell-autonomous machinery governing the cancer cell inflammatory output in response to immunogenic therapies remains poorly defined. Here, we profiled the transcriptome of cancer cells responding to immunogenic or weakly immunogenic treatments. Bioinformatics-driven pathway analysis indicated that immunogenic treatments instigated a NF-κB/AP-1-i"],"journal":["Cell death and differentiation"],"pubmed_title":["Stress-induced inflammation evoked by immunogenic cell death is blunted by the IRE1α kinase inhibitor KIRA6 through HSP60 targeting."],"pmcid":["PMC8738768"],"funding_grant_id":["T 974"],"pubmed_authors":["Sinkkonen L","Korovesis D","Garg AD","Vara-Perez M","Finotello F","de Witte PA","Van Eygen S","Rozanc J","Janssens S","Derua R","Dewaele M","Alexopoulos LG","Rufo N","Verhelst SHL","Sauter T","Agostinis P"],"additional_accession":[]},"is_claimable":false,"name":"Stress-induced inflammation evoked by immunogenic cell death is blunted by the IRE1α kinase inhibitor KIRA6 through HSP60 targeting.","description":"Mounting evidence indicates that immunogenic therapies engaging the unfolded protein response (UPR) following endoplasmic reticulum (ER) stress favor proficient cancer cell-immune interactions, by stimulating the release of immunomodulatory/proinflammatory factors by stressed or dying cancer cells. UPR-driven transcription of proinflammatory cytokines/chemokines exert beneficial or detrimental effects on tumor growth and antitumor immunity, but the cell-autonomous machinery governing the cancer cell inflammatory output in response to immunogenic therapies remains poorly defined. Here, we profiled the transcriptome of cancer cells responding to immunogenic or weakly immunogenic treatments. Bioinformatics-driven pathway analysis indicated that immunogenic treatments instigated a NF-κB/AP-1-i","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-05-28T23:38:07.75Z","creation":"2022-02-11T16:11:33.202Z"},"accession":"S-EPMC8738768","cross_references":{"pubmed":["34453119"],"doi":["10.1038/s41418-021-00853-5"]}}