Open AccessRetracted: 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI 3K/ AKT signaling
Author(s) -
Li Junjun,
Xu Hao,
Wang Qiangping,
Wang Sihua,
Xiong Nanxiang
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1950
Subject(s) - snail , protein kinase b , pi3k/akt/mtor pathway , gene knockdown , glioma , cancer research , western blot , biology , cell migration , cell growth , signal transduction , blot , cell , microbiology and biotechnology , cell culture , gene , genetics , ecology
Abstract 14‐3‐3ζ has been reported to function as critical regulators of diverse cellular responses. However, the role of 14‐3‐3ζ in gliomas progression remains largely unknown. The expression level of 14‐3‐3ζ and Snail was detected by Western blot analysis and quantitative polymerase chain reaction in different grades of human gliomas. The effect of 14‐3‐3ζ on gliomas progression was measured using cell migration and invasion assay, the colony formation experiment, and CCK ‐8 assay. The effect of 14‐3‐3ζ on PI 3K/ AKT /Snail signaling protein expression levels was tested by Western blotting. Firstly, 14‐3‐3ζ 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 14‐3‐3ζ promoted gliomas cells proliferation, migration, and invasion. Conversely, the knockdown of 14‐3‐3ζ suppressed gliomas cells proliferation, migration, and invasion. Furthermore, subsequent mechanistic studies showed that 14‐3‐3ζ could activate PI 3K/ AKT / Snail signaling pathway to facilitate gliomas cells proliferation, migration, and invasion. This study shows that the overexpression of 14‐3‐3ζ can promote remarkably gliomas cells proliferation, migration, and invasion by regulating the Snail protein expression through activating PI 3K/ AKT signaling, and it may serve as a potential prognostic marker and therapeutic target for gliomas.