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

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 diffe...

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Autores principales: Li, Junjun, Xu, Hao, Wang, Qiangping, Wang, Sihua, Xiong, Nanxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382716/
https://www.ncbi.nlm.nih.gov/pubmed/30656845
http://dx.doi.org/10.1002/cam4.1950
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author Li, Junjun
Xu, Hao
Wang, Qiangping
Wang, Sihua
Xiong, Nanxiang
author_facet Li, Junjun
Xu, Hao
Wang, Qiangping
Wang, Sihua
Xiong, Nanxiang
author_sort Li, Junjun
collection PubMed
description 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.
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spelling pubmed-63827162019-03-01 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling Li, Junjun Xu, Hao Wang, Qiangping Wang, Sihua Xiong, Nanxiang Cancer Med Cancer Biology 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. John Wiley and Sons Inc. 2019-01-18 /pmc/articles/PMC6382716/ /pubmed/30656845 http://dx.doi.org/10.1002/cam4.1950 Text en © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Cancer Biology
Li, Junjun
Xu, Hao
Wang, Qiangping
Wang, Sihua
Xiong, Nanxiang
14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title_full 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title_fullStr 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title_full_unstemmed 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title_short 14‐3‐3ζ promotes gliomas cells invasion by regulating Snail through the PI3K/AKT signaling
title_sort 14‐3‐3ζ promotes gliomas cells invasion by regulating snail through the pi3k/akt signaling
topic Cancer Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382716/
https://www.ncbi.nlm.nih.gov/pubmed/30656845
http://dx.doi.org/10.1002/cam4.1950
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