GLIS family zinc finger 3 promoting cell malignant behaviors and NF-κB signaling in glioma

• Published in: Brain research 2021-11, Vol.1770, p.147623-147623, Article 147623
• Main Authors: Liu, Zhuohang, Liu, Luochen, Qi, Yanan, Li, Hang, Pan, Shuyi
• Format: Article
• Language: English
• Subjects: Animals; Brain Neoplasms - genetics; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Cell Line, Tumor; Cell Proliferation - genetics; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Gene Expression Regulation, Neoplastic; Glioma; Glioma - genetics; Glioma - metabolism; Glioma - pathology; GLIS3; Humans; Male; Mice; Mice, Nude; NF-kappa B - metabolism; NF-κB; Repressor Proteins - genetics; Repressor Proteins - metabolism; Signal Transduction - genetics; Trans-Activators - genetics; Trans-Activators - metabolism
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2021.147623

[Display omitted] •GLIS3 promotes glioma cell proliferation, migration and invasion through the regulation of NF-κB pathway. Glioma is a common tumor in the human central nervous system. However, its molecular mechanism in the pathogenesis and regulation of glioma progression is still unclear. In this study, we found that GLIS3 was up-regulated in glioma tissues, and the increased expression is positively correlated with advanced tumor grade. Survival evaluation disclosed that patients with high expression levels of GLIS3 normally have a poor prognosis. Functional analysis revealed the oncogenic role of GLIS3 in the development of glioma. GLIS3 promotes glioma cells’ invasion, migration, and proliferation. Meanwhile, deficiency of GLIS3 produces an inhibitory function upon NF-κB signaling pathway. This work demonstrated that GLIS3, acting as a target and prognostic factor for glioma, may promote the invasion, migration and proliferation of glioma cells involved in regulation of NF-κB signaling pathway.