Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. [[Kinesin]] superfamily protein 4 (KIF4), a KIF member classified in [[Kinesin]] 4 has been indicated as a mediator acted in the [[tumorigenesis]] of human [[cancer]]. The mechanism of [[KIF4A]] in [[glioma]] is yet to be investigated. Zhang et al. explored the potential function and mechanism of KIF4A in gliomas. They analyzed the KIF4A expression and the prognosis in glioma patients using [[The Cancer Genome Atlas]] (TCGA) databases. KIF4A levels in normal human [[astrocyte]] cell (NHA) and glioma cell lines were examined by [[Western blot]]. They studied the function of KIF4A on proliferation, migration, invasion, and cell cycle in glioma cell lines using a series of in vitro and in vivo experiments. Chromatin Immunoprecipitation (ChIP) analysis was applied to search potential KIF4A related downstream in glioma. They identified the significantly up-regulated expression of KIF4A both in glioma tissues and cells. Glioma patients with elevated KIF4A expression have shorter survival. Down-regulation of KIF4A exerted an inhibitory effect on cell proliferation, invasion, and migration. We crucially identified that KIF4A drives glioma growth by transcriptional repression of Rac1/Cdc42 to induce cytoskeletal remodeling in [[glioma cell]]s. [[Knockdown]] of KIF4A decreased [[RohA]], [[Rac1]], [[Cdc42]], [[Pak1]] and [[Pak2]] expression level. The study provided a prospect that KIF4A functions as an [[oncogene]] in glioma ((Zhang H, Meng S, Chu K, Chu S, Fan YC, Bai J, Yu ZQ. KIF4A drives glioma growth by transcriptional repression of Rac1/Cdc42 to induce cytoskeletal remodeling in glioma cells. J Cancer. 2022 Nov 21;13(15):3640-3651. doi: 10.7150/jca.77238. PMID: 36606197; PMCID: PMC9809311.)). pak2.txt Last modified: 2024/06/07 02:55by 127.0.0.1