TMIC-12. COMPLEMENT SIGNALING IN HYPOXIC NICHES OF THE GLIOMA MICROENVIRONMENT
نویسندگان
چکیده
Abstract Glioblastoma is the most common and aggressive primary brain tumor in adults. Despite treatment through surgery, irradiation chemotherapy, all patients suffer recurrence of treatment-resistant tumors. Previous studies from our lab showed that astrocytes become reactive generate tumor-supportive conditions for glioma cells, when exposed to hypoxia or irradiation. Reactive are known upregulate proteins complement system, especially component 3 (C3), several neurological disorders. However, it remains unexplored how these expressed stromal glioblastoma. Tissue sections a mouse model presence C3 invasive front, hypoxic, perivascular spaces tumors, where there an abundance astrocytes. expression co-localized with Nestin CD44, two markers mesenchymal and/or stem-like cells. Primary human grown hypoxic upregulated as well other associated more extensive infiltrative phenotype In general, strong correlation between (195 genes) (200 gene signatures were found TCGA GBM dataset (R= 0.82, p-value= 0). Single-cell sequencing data tumors subpopulation highly C3-expressing astrocytes, which enriched cellular pathways comprising epithelial transition (EMT), TNF-alpha, complement, hypoxia, interferon signaling. Human cell lines proneural, classical subtypes increased CAIX GLUT1 under lower oxygen tensions, while out three upregulation stemness (OCT4 NANOG1) C3aR. Overall, indicate link microenvironment, local could possibly lead promoting signaling, will be further explored.
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ژورنال
عنوان ژورنال: Neuro-oncology
سال: 2022
ISSN: ['1523-5866', '1522-8517']
DOI: https://doi.org/10.1093/neuonc/noac209.1056