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IFI35 regulates non-canonical NF-κB signaling to maintain glioblastoma stem cells and recruit tumor-associated macrophages
Journal article   Peer reviewed

IFI35 regulates non-canonical NF-κB signaling to maintain glioblastoma stem cells and recruit tumor-associated macrophages

Daqi Li, Xiefeng Wang, Kexin Chen, Danyang Shan, Gaoyuan Cui, Wei Yuan, Qiankun Lin, Ryan C. Gimple, Deobrat Dixit, Chenfei Lu, …
Cell death and differentiation, Vol.31(6), pp.738-752
06/01/2024
DOI: 10.1038/s41418-024-01292-8
PMCID: PMC11165006
PMID: 38594444
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC11165006/pdf/41418_2024_Article_1292.pdfView
Open Access

Abstract

Glioblastoma (GBM) is the most aggressive malignant primary brain tumor characterized by a highly heterogeneous and immunosuppressive tumor microenvironment (TME). The symbiotic interactions between glioblastoma stem cells (GSCs) and tumor-associated macrophages (TAM) in the TME are critical for tumor progression. Here, we identified that IFI35, a transcriptional regulatory factor, plays both cell-intrinsic and cell-extrinsic roles in maintaining GSCs and the immunosuppressive TME. IFI35 induced non-canonical NF-kB signaling through proteasomal processing of p105 to the DNA-binding transcription factor p50, which heterodimerizes with RELB (RELB/p50), and activated cell chemotaxis in a cell-autonomous manner. Further, IFI35 induced recruitment and maintenance of M2-like TAMs in TME in a paracrine manner. Targeting IFI35 effectively suppressed in vivo tumor growth and prolonged survival of orthotopic xenograft-bearing mice. Collectively, these findings reveal the tumor-promoting functions of IFI35 and suggest that targeting IFI35 or its downstream effectors may provide effective approaches to improve GBM treatment.
Cell Biology Biochemistry & Molecular Biology Life Sciences & Biomedicine Science & Technology

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