14-3-3 zeta promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling

14-3-3 zeta has been reported to function as critical regulators of diverse cellular responses. However, the role of 14-3-3 zeta in gliomas progression remains largely unknown. The expression level of 14-3-3 zeta and Snail was detected by Western blot analysis and quantitative polymerase chain reaction in different grades of human gliomas. The effect of 14-3-3 zeta on gliomas progression was measured using cell migration and invasion assay, the colony formation experiment, and CCK-8 assay. The effect of 14-3-3 zeta on PI3K/AKT/Snail signaling protein expression levels was tested by Western blotting. Firstly, 14-3-3 zeta was often up-regulated in high-grade gliomas relative to low-grade gliomas, and this overexpression was significantly related to tumor size, Karnofsky Performance Scale score and weaker disease-free survival. Secondly, the overexpression of 14-3-3 zeta promoted gliomas cells proliferation, migration, and invasion. Conversely, the knockdown of 14-3-3 zeta suppressed gliomas cells proliferation, migration, and invasion. Furthermore, subsequent mechanistic studies showed that 14-3-3 zeta could activate PI3K/AKT/Snail signaling pathway to facilitate gliomas cells proliferation, migration, and invasion. This study shows that the overexpression of 14-3-3 zeta can promote remarkably gliomas cells proliferation, migration, and invasion by regulating the Snail protein expression through activating PI3K/AKT signaling, and it may serve as a potential prognostic marker and therapeutic target for gliomas.