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Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation

This current study tested expression and potential biological functions of Gab3 in human glioma. Gab3 mRNA and protein expression was significantly elevated in human glioma tissues and glioma cells. Its level was however low in normal brain tissues and primary human astrocytes. In both established (...

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Detalles Bibliográficos
Autores principales: Jia, Pifeng, Li, Feng, Gu, Weiting, Zhang, Weifeng, Cai, Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349442/
https://www.ncbi.nlm.nih.gov/pubmed/28291820
http://dx.doi.org/10.1371/journal.pone.0173473
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author Jia, Pifeng
Li, Feng
Gu, Weiting
Zhang, Weifeng
Cai, Yu
author_facet Jia, Pifeng
Li, Feng
Gu, Weiting
Zhang, Weifeng
Cai, Yu
author_sort Jia, Pifeng
collection PubMed
description This current study tested expression and potential biological functions of Gab3 in human glioma. Gab3 mRNA and protein expression was significantly elevated in human glioma tissues and glioma cells. Its level was however low in normal brain tissues and primary human astrocytes. In both established (U251MG cell line) and primary human glioma cells, Gab3 knockdown by shRNA/siRNA significantly inhibited Akt activation and cell proliferation. Reversely, forced Gab3 overexpression in U251MG cells promoted Akt activation and cell proliferation. In vivo, the growth of U251MG tumors in nude mice was inhibited following expressing Gab3 shRNA. Akt activation in cancer tissues was also suppressed by Gab3 shRNA. Together, we conclude that Gab3 overexpression in human glioma mediates Akt activation and cancer cell proliferation.
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spelling pubmed-53494422017-04-06 Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation Jia, Pifeng Li, Feng Gu, Weiting Zhang, Weifeng Cai, Yu PLoS One Research Article This current study tested expression and potential biological functions of Gab3 in human glioma. Gab3 mRNA and protein expression was significantly elevated in human glioma tissues and glioma cells. Its level was however low in normal brain tissues and primary human astrocytes. In both established (U251MG cell line) and primary human glioma cells, Gab3 knockdown by shRNA/siRNA significantly inhibited Akt activation and cell proliferation. Reversely, forced Gab3 overexpression in U251MG cells promoted Akt activation and cell proliferation. In vivo, the growth of U251MG tumors in nude mice was inhibited following expressing Gab3 shRNA. Akt activation in cancer tissues was also suppressed by Gab3 shRNA. Together, we conclude that Gab3 overexpression in human glioma mediates Akt activation and cancer cell proliferation. Public Library of Science 2017-03-14 /pmc/articles/PMC5349442/ /pubmed/28291820 http://dx.doi.org/10.1371/journal.pone.0173473 Text en © 2017 Jia et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Jia, Pifeng
Li, Feng
Gu, Weiting
Zhang, Weifeng
Cai, Yu
Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title_full Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title_fullStr Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title_full_unstemmed Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title_short Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation
title_sort gab3 overexpression in human glioma mediates akt activation and tumor cell proliferation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349442/
https://www.ncbi.nlm.nih.gov/pubmed/28291820
http://dx.doi.org/10.1371/journal.pone.0173473
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