TY - JOUR AU - Man, Ka Hou AU - Wu, Yonghe AU - Gao, Zhenjiang AU - Spreng, Anna-Sophie AU - Keding, Sigrun Johanna Elisabeth AU - Mangei, Jasmin AU - Boskovic, Pavle AU - Mallm, Jan-Philipp AU - Liu, Hai-Kun AU - Imbusch, Charles D AU - Lichter, Peter AU - Radlwimmer, Bernhard TI - SOX10 mediates glioblastoma cell-state plasticity. JO - EMBO reports VL - 25 IS - 11 SN - 1469-221X CY - Hoboken, NJ [u.a.] PB - Wiley M1 - DKFZ-2024-01877 SP - 5113-5140 PY - 2024 N1 - #EA:B060#LA:B060# / 2024 Nov;25(11):5113-5140 AB - Phenotypic plasticity is a cause of glioblastoma therapy failure. We previously showed that suppressing the oligodendrocyte-lineage regulator SOX10 promotes glioblastoma progression. Here, we analyze SOX10-mediated phenotypic plasticity and exploit it for glioblastoma therapy design. We show that low SOX10 expression is linked to neural stem-cell (NSC)-like glioblastoma cell states and is a consequence of temozolomide treatment in animal and cell line models. Single-cell transcriptome profiling of Sox10-KD tumors indicates that Sox10 suppression is sufficient to induce tumor progression to an aggressive NSC/developmental-like phenotype, including a quiescent NSC-like cell population. The quiescent NSC state is induced by temozolomide and Sox10-KD and reduced by Notch pathway inhibition in cell line models. Combination treatment using Notch and HDAC/PI3K inhibitors extends the survival of mice carrying Sox10-KD tumors, validating our experimental therapy approach. In summary, SOX10 suppression mediates glioblastoma progression through NSC/developmental cell-state transition, including the induction of a targetable quiescent NSC state. This work provides a rationale for the design of tumor therapies based on single-cell phenotypic plasticity analysis. KW - SOX10 (Other) KW - Glioblastoma (Other) KW - Phenotypic Plasticity (Other) KW - Therapy Resistance (Other) KW - Tumor Cell Quiescence (Other) LB - PUB:(DE-HGF)16 C6 - pmid:39285246 DO - DOI:10.1038/s44319-024-00258-8 UR - https://inrepo02.dkfz.de/record/293327 ER -