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SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma
The suppressor of zest 12 (SUZ12), one of the core polycomb repressive complex 2 (PRC2) components, has increasingly appreciated as a key mediator during human tumorigenesis. However, its expression pattern and oncogenic roles in head and neck squamous cell carcinoma (HNSCC) remain largely unexplore...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6010759/ https://www.ncbi.nlm.nih.gov/pubmed/29667751 http://dx.doi.org/10.1111/jcmm.13638 |
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author | Wu, Yaping Hu, Huijun Zhang, Wei Li, Zhongwu Diao, Pengfei Wang, Dongmiao Zhang, Wei Wang, Yanling Yang, Jianrong Cheng, Jie |
author_facet | Wu, Yaping Hu, Huijun Zhang, Wei Li, Zhongwu Diao, Pengfei Wang, Dongmiao Zhang, Wei Wang, Yanling Yang, Jianrong Cheng, Jie |
author_sort | Wu, Yaping |
collection | PubMed |
description | The suppressor of zest 12 (SUZ12), one of the core polycomb repressive complex 2 (PRC2) components, has increasingly appreciated as a key mediator during human tumorigenesis. However, its expression pattern and oncogenic roles in head and neck squamous cell carcinoma (HNSCC) remain largely unexplored yet. Here, we sought to determine its expression pattern, clinicopathological significance and biological roles in HNSCC. Through data mining and interrogation from multiple publicly available databases, our bioinformatics analyses revealed that SUZ12 mRNA was significantly overexpressed in multiple HNSCC patient cohorts. Moreover, SUZ12 protein was markedly up‐regulated in primary HNSCC samples from our patient cohort as assessed by immunohistochemical staining and its overexpression significantly associated with cervical node metastasis and reduced overall and disease‐free survival. In the 4‐nitroquinoline 1‐oxide (4NQO)‐induced HNSCC mouse model, increased SUZ12 immunostaining was observed along with disease progression from epithelial hyperplasia to squamous cell carcinoma in tongue. Furthermore, shRNA‐mediated SUZ12 knock‐down significantly inhibited cell proliferation, migration and invasion in HNSCC cells, and resulted in compromised tumour growth in vivo. Collectively, our data reveal that SUZ12 might serve as a putative oncogene by promoting cell proliferation, migration and invasion, and also a novel biomarker with diagnostic and prognostic significance for HNSCC. |
format | Online Article Text |
id | pubmed-6010759 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60107592018-07-01 SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma Wu, Yaping Hu, Huijun Zhang, Wei Li, Zhongwu Diao, Pengfei Wang, Dongmiao Zhang, Wei Wang, Yanling Yang, Jianrong Cheng, Jie J Cell Mol Med Original Articles The suppressor of zest 12 (SUZ12), one of the core polycomb repressive complex 2 (PRC2) components, has increasingly appreciated as a key mediator during human tumorigenesis. However, its expression pattern and oncogenic roles in head and neck squamous cell carcinoma (HNSCC) remain largely unexplored yet. Here, we sought to determine its expression pattern, clinicopathological significance and biological roles in HNSCC. Through data mining and interrogation from multiple publicly available databases, our bioinformatics analyses revealed that SUZ12 mRNA was significantly overexpressed in multiple HNSCC patient cohorts. Moreover, SUZ12 protein was markedly up‐regulated in primary HNSCC samples from our patient cohort as assessed by immunohistochemical staining and its overexpression significantly associated with cervical node metastasis and reduced overall and disease‐free survival. In the 4‐nitroquinoline 1‐oxide (4NQO)‐induced HNSCC mouse model, increased SUZ12 immunostaining was observed along with disease progression from epithelial hyperplasia to squamous cell carcinoma in tongue. Furthermore, shRNA‐mediated SUZ12 knock‐down significantly inhibited cell proliferation, migration and invasion in HNSCC cells, and resulted in compromised tumour growth in vivo. Collectively, our data reveal that SUZ12 might serve as a putative oncogene by promoting cell proliferation, migration and invasion, and also a novel biomarker with diagnostic and prognostic significance for HNSCC. John Wiley and Sons Inc. 2018-04-18 2018-07 /pmc/articles/PMC6010759/ /pubmed/29667751 http://dx.doi.org/10.1111/jcmm.13638 Text en © 2018 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 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 Wu, Yaping Hu, Huijun Zhang, Wei Li, Zhongwu Diao, Pengfei Wang, Dongmiao Zhang, Wei Wang, Yanling Yang, Jianrong Cheng, Jie SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title |
SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title_full |
SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title_fullStr |
SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title_full_unstemmed |
SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title_short |
SUZ12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
title_sort | suz12 is a novel putative oncogene promoting tumorigenesis in head and neck squamous cell carcinoma |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6010759/ https://www.ncbi.nlm.nih.gov/pubmed/29667751 http://dx.doi.org/10.1111/jcmm.13638 |
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