%0 Journal Article
%T Paromomycin Inhibits HDAC1-Dependent SUMOylation and IGF1R Membrane Translocation in Glioblastoma
%A Sarah Mitchell
%A Olivia Brown
%A James Walker
%J Specialty Journal of Pharmacognosy, Phytochemistry, and Biotechnology
%@ 3062-441X
%D 2023
%V 3
%N 1
%R 10.51847/ZlSy1ptrQD
%P 93-115
%X This work explores how Paromomycin influences SUMOylation-associated signaling in glioblastoma (GBM), with a particular focus on its inhibitory action on HDAC1. SUMOylation-related genes linked to GBM outcomes were screened using TCGA and GTEx datasets. Molecular docking predicted Paromomycin as a likely HDAC1 inhibitor. Functional experiments in U-251MG GBM cells—including CCK8 viability assays, qRT-PCR, and immunofluorescence—were conducted to evaluate its impact on SUMOylation gene activity, cell growth, and IGF1R trafficking. Paromomycin reduced GBM cell survival, colony formation, and migratory capacity in a concentration-dependent manner. It altered SUMO1 expression and suppressed IGF1R entry into the nucleus, an effect counteracted by the HDAC1 inhibitor Trichostatin A (TSA), supporting a role for Paromomycin in SUMO1-dependent regulatory mechanisms. These findings position Paromomycin as a promising GBM therapeutic candidate through its modulation of HDAC1-driven SUMOylation processes and regulation of IGF1R nuclear transport, emphasizing the need for further clinical-oriented studies.
%U https://galaxypub.co/article/paromomycin-inhibits-hdac1-dependent-sumoylation-and-igf1r-membrane-translocation-in-glioblastoma-kh0xweya2nchpnk