Jian-Ying Chuang

Abstract The interaction between glioblastoma cells and glioblastoma-associated macrophages (GAMs) influences the immunosuppressive tumor microenvironment, leading to ineffective immunotherapies. We hypothesized that disrupting the communication between tumors and macrophages would enhance the efficacy of immunotherapies. Transcriptomic analysis of recurrent glioblastoma specimens indicated an enhanced neuroinflammatory pathway, with CXCL12 emerging as the top-ranked gene in secretory molecules.

In this study, we showed that SH3GLB1 could affect spheroid formation and regulate CD133 expression through H4K5 acetylation of the promoter (Fig. 6). The findings show that the GBM-resistant cells with high SH3GLB1 levels can contribute to enhanced TIC-features, such as genes and morphology, leading to an increase in cell resistance to drug treatment. The schematic diagram illustrates the role of SH3GLB1 on spheroid formation and regulation of CD133 transcription in GBM cells. GBM: Glioblastoma

ABSTRACT In a subgroup of patients with amyotrophic lateral sclerosis (ALS)/Frontotemporal dementia (FTD), the (G4C2)-RNA repeat expansion from C9orf72 chromosome binds to the Ran-activating protein (RanGAP) at the nuclear pore, resulting in nucleocytoplasmic transport deficit and accumulation of Ran in the cytosol. Here, we found that the sigma-1 receptor (Sig-1R), a molecular chaperone, reverses the pathological effects of (G4C2)-RNA repeats in cell lines and in Drosophila.