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Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling
SH3GL2 (Src homology 3 (SH3) domain GRB2‐like 2) is mainly expressed in the central nervous system and regarded as a tumour suppressor in human glioma. However, the molecular mechanism of the SH3GL2 protein involved in malignant behaviours of human glioma has not been elucidated. In this study, we t...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661104/ https://www.ncbi.nlm.nih.gov/pubmed/28470949 http://dx.doi.org/10.1111/jcmm.13184 |
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author | Zhu, Yufu Zhang, Xiang Wang, Lei Ji, Zhe Xie, Manyi Zhou, Xinyu Liu, Zhiyi Shi, Hengliang Yu, Rutong |
author_facet | Zhu, Yufu Zhang, Xiang Wang, Lei Ji, Zhe Xie, Manyi Zhou, Xinyu Liu, Zhiyi Shi, Hengliang Yu, Rutong |
author_sort | Zhu, Yufu |
collection | PubMed |
description | SH3GL2 (Src homology 3 (SH3) domain GRB2‐like 2) is mainly expressed in the central nervous system and regarded as a tumour suppressor in human glioma. However, the molecular mechanism of the SH3GL2 protein involved in malignant behaviours of human glioma has not been elucidated. In this study, we tried to investigate the role of SH3GL2 in glioma cell migration and invasion and explore its underlined molecular mechanism. Firstly, we discovered that the protein level of SH3GL2 was widely decreased in the human glioma patients, especially in high‐grade glioma tissues. Then, we determined the role of SH3GL2 in migration and invasion of glioma cells upon SH3GL2 knocking down and overexpressing. It was showed that knocking down of SH3GL2 promoted the migration and invasion of glioma cells, whereas overexpression of SH3GL2 inhibited them. Further study on molecular mechanism disclosed that silencing of SH3GL2 obviously activated the STAT3 (signal transducer and activator of transcription 3) signalling thereby promoting the expression and secretion of MMP2. On the contrary, overexpression of SH3GL2 had opposite effect. Taken together, the above results suggest that SH3GL2 suppresses migration and invasion behaviours of glioma cells through negatively regulating STAT3/MMP2 signalling and that loss of SH3GL2 may intensify the STAT3/MMP2 signalling thereby contributing to the migration and invasion of glioma cells. |
format | Online Article Text |
id | pubmed-5661104 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-56611042017-11-02 Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling Zhu, Yufu Zhang, Xiang Wang, Lei Ji, Zhe Xie, Manyi Zhou, Xinyu Liu, Zhiyi Shi, Hengliang Yu, Rutong J Cell Mol Med Original Articles SH3GL2 (Src homology 3 (SH3) domain GRB2‐like 2) is mainly expressed in the central nervous system and regarded as a tumour suppressor in human glioma. However, the molecular mechanism of the SH3GL2 protein involved in malignant behaviours of human glioma has not been elucidated. In this study, we tried to investigate the role of SH3GL2 in glioma cell migration and invasion and explore its underlined molecular mechanism. Firstly, we discovered that the protein level of SH3GL2 was widely decreased in the human glioma patients, especially in high‐grade glioma tissues. Then, we determined the role of SH3GL2 in migration and invasion of glioma cells upon SH3GL2 knocking down and overexpressing. It was showed that knocking down of SH3GL2 promoted the migration and invasion of glioma cells, whereas overexpression of SH3GL2 inhibited them. Further study on molecular mechanism disclosed that silencing of SH3GL2 obviously activated the STAT3 (signal transducer and activator of transcription 3) signalling thereby promoting the expression and secretion of MMP2. On the contrary, overexpression of SH3GL2 had opposite effect. Taken together, the above results suggest that SH3GL2 suppresses migration and invasion behaviours of glioma cells through negatively regulating STAT3/MMP2 signalling and that loss of SH3GL2 may intensify the STAT3/MMP2 signalling thereby contributing to the migration and invasion of glioma cells. John Wiley and Sons Inc. 2017-05-04 2017-11 /pmc/articles/PMC5661104/ /pubmed/28470949 http://dx.doi.org/10.1111/jcmm.13184 Text en © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (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 | Original Articles Zhu, Yufu Zhang, Xiang Wang, Lei Ji, Zhe Xie, Manyi Zhou, Xinyu Liu, Zhiyi Shi, Hengliang Yu, Rutong Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title | Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title_full | Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title_fullStr | Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title_full_unstemmed | Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title_short | Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling |
title_sort | loss of sh3gl2 promotes the migration and invasion behaviours of glioblastoma cells through activating the stat3/mmp2 signalling |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661104/ https://www.ncbi.nlm.nih.gov/pubmed/28470949 http://dx.doi.org/10.1111/jcmm.13184 |
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