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- W3035529059 abstract "Abstract The interplay between glioblastoma stem cells (GSCs) and tumor-associated macrophages (TAMs) promotes progression of glioblastoma multiforme (GBM). However, the detailed molecular mechanisms underlying the relationship between these two cell types remain unclear. Here, we demonstrate that ARS2 (arsenite-resistance protein 2), a zinc finger protein that is essential for early mammalian development, plays critical roles in GSC maintenance and M2-like TAM polarization. ARS2 directly activates its novel transcriptional target MGLL , encoding monoacylglycerol lipase (MAGL), to regulate the self-renewal and tumorigenicity of GSCs through production of prostaglandin E 2 (PGE 2 ), which stimulates β-catenin activation of GSC and M2-like TAM polarization. We identify M2-like signature downregulated by which MAGL-specific inhibitor, JZL184, increased survival rate significantly in the mouse xenograft model by blocking PGE 2 production. Taken together, our results suggest that blocking the interplay between GSCs and TAMs by targeting ARS2/MAGL signaling offers a potentially novel therapeutic option for GBM patients." @default.
- W3035529059 created "2020-06-19" @default.
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- W3035529059 date "2020-06-12" @default.
- W3035529059 modified "2023-10-16" @default.
- W3035529059 title "ARS2/MAGL signaling in glioblastoma stem cells promotes self-renewal and M2-like polarization of tumor-associated macrophages" @default.
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- W3035529059 doi "https://doi.org/10.1038/s41467-020-16789-2" @default.
- W3035529059 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7293269" @default.
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