{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Wicher G"],"pubmed_abstract":["<h4>Background</h4>Glioblastoma (GBM) is the most common primary malignant brain tumor in adults, characterized by aggressive growth and a dismal prognosis. Interleukin-33 (IL-33) and its receptor ST2 have emerged as regulators of glioma growth, but their exact function in tumorigenesis has not been deciphered. Indeed, previous studies on IL-33 in cancer have yielded somewhat opposing results as to whether it is pro- or anti-tumorigenic.<h4>Methods</h4>IL-33 expression was assessed in a GBM tissue microarray and public databases. As in vivo models we used orthotopic xenografts of patient-derived GBM cells, and syngenic models with grafted mouse glioma cells.<h4>Results</h4>We analyzed the role of IL-33 and its receptor ST2 in nonmalignant cells of the glioma microenvironment and found that IL-33 levels are increased in cells surrounding the tumor. Protein complexes of IL-33 and ST2 are mainly found outside of the tumor core. The IL-33-producing cells consist primarily of oligodendrocytes. To determine the function of IL-33 in the tumor microenvironment, we used mice lacking the ST2 receptor. When glioma cells were grafted to ST2-deficient mouse brains, the resulting tumors exhibited a more invasive growth pattern, and are associated with poorer survival, compared to <i>wild-type</i> mice. Tumors in ST2-deficient hosts are more invasive, with increased expression of extracellular matrix remodeling enzymes and enhanced tumor angiogenesis. Furthermore, the absence of ST2 leads to a more immunosuppressive environment.<h4>Conclusions</h4>Our findings reveal that glia-derived IL-33 and its receptor ST2 participate in modulating tumor invasiveness, tumor vasculature, and immunosuppression in glioma."],"journal":["Neuro-oncology advances"],"pagination":["vdaf010"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11808570"],"repository":["biostudies-literature"],"pubmed_title":["Lack of ST2 aggravates glioma invasiveness, vascular abnormality, and immune suppression."],"pmcid":["PMC11808570"],"pubmed_authors":["Vaccaro A","Imbria RN","Wicher G","Vemuri K","Roy A","Ramachandran M","Olofsson T","Nilsson G","Belting M","Forsberg-Nilsson K","Dimberg A"],"additional_accession":[]},"is_claimable":false,"name":"Lack of ST2 aggravates glioma invasiveness, vascular abnormality, and immune suppression.","description":"<h4>Background</h4>Glioblastoma (GBM) is the most common primary malignant brain tumor in adults, characterized by aggressive growth and a dismal prognosis. Interleukin-33 (IL-33) and its receptor ST2 have emerged as regulators of glioma growth, but their exact function in tumorigenesis has not been deciphered. Indeed, previous studies on IL-33 in cancer have yielded somewhat opposing results as to whether it is pro- or anti-tumorigenic.<h4>Methods</h4>IL-33 expression was assessed in a GBM tissue microarray and public databases. As in vivo models we used orthotopic xenografts of patient-derived GBM cells, and syngenic models with grafted mouse glioma cells.<h4>Results</h4>We analyzed the role of IL-33 and its receptor ST2 in nonmalignant cells of the glioma microenvironment and found that IL-33 levels are increased in cells surrounding the tumor. Protein complexes of IL-33 and ST2 are mainly found outside of the tumor core. The IL-33-producing cells consist primarily of oligodendrocytes. To determine the function of IL-33 in the tumor microenvironment, we used mice lacking the ST2 receptor. When glioma cells were grafted to ST2-deficient mouse brains, the resulting tumors exhibited a more invasive growth pattern, and are associated with poorer survival, compared to <i>wild-type</i> mice. Tumors in ST2-deficient hosts are more invasive, with increased expression of extracellular matrix remodeling enzymes and enhanced tumor angiogenesis. Furthermore, the absence of ST2 leads to a more immunosuppressive environment.<h4>Conclusions</h4>Our findings reveal that glia-derived IL-33 and its receptor ST2 participate in modulating tumor invasiveness, tumor vasculature, and immunosuppression in glioma.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan-Dec","modification":"2025-04-04T02:56:48.14Z","creation":"2025-04-04T02:56:48.14Z"},"accession":"S-EPMC11808570","cross_references":{"pubmed":["39931535"],"doi":["10.1093/noajnl/vdaf010"]}}