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


Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
02 2019
Historique:
received: 08 08 2018
revised: 12 11 2018
accepted: 10 12 2018
pubmed: 19 1 2019
medline: 27 3 2020
entrez: 19 1 2019
Statut: ppublish

Résumé

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 PI3K/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 PI3K/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 PI3K/AKT signaling, and it may serve as a potential prognostic marker and therapeutic target for gliomas.

Identifiants

pubmed: 30656845
doi: 10.1002/cam4.1950
pmc: PMC6382716
doi:

Substances chimiques

14-3-3 Proteins 0
RNA, Messenger 0
Snail Family Transcription Factors 0
YWHAZ protein, human 0
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't Retracted Publication

Langues

eng

Sous-ensembles de citation

IM

Pagination

783-794

Commentaires et corrections

Type : RetractionIn

Informations de copyright

© 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

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Auteurs

Junjun Li (J)

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Hao Xu (H)

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Qiangping Wang (Q)

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Sihua Wang (S)

Department of Thoracic surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Nanxiang Xiong (N)

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

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Classifications MeSH