Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

Abstract Centrosomal protein 55 (CEP55) is a microtubule-bundling protein that participants in cell mitosis. It is overexpressed in several solid tumours and promotes the growth and invasion of cancer cells. However, the role of CEP55 in pancreatic cancer (PANC) remains unclear. Herein, upregulated...

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Autores principales:	Tao Peng, Wei Zhou, Feng Guo, He-shui Wu, Chun-you Wang, Li Wang, Zhi-yong Yang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8617f4b80f9240a28f206e041b2c95f0
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spelling	oai:doaj.org-article:8617f4b80f9240a28f206e041b2c95f02021-12-02T11:52:58ZCentrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness10.1038/s41598-017-06132-z2045-2322https://doaj.org/article/8617f4b80f9240a28f206e041b2c95f02017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06132-zhttps://doaj.org/toc/2045-2322Abstract Centrosomal protein 55 (CEP55) is a microtubule-bundling protein that participants in cell mitosis. It is overexpressed in several solid tumours and promotes the growth and invasion of cancer cells. However, the role of CEP55 in pancreatic cancer (PANC) remains unclear. Herein, upregulated expression of CEP55 (associated with poor prognosis) was detected in PANC using quantitative real-time reverse transcription PCR, western blotting, and immunohistochemistry. Cell migration, colony formation, wound-healing, and Transwell matrix penetration assays, revealed that upregulation of CEP55 promoted PANC cells proliferation, migration, and invasion in vitro, whereas knockdown of CEP55 attenuated it. In an in vivo murine model, CEP55 overexpression accelerated PANC cells tumourigenicity, together with upregulation of the protein levels of invasion-related proteins matrix metalloproteinase (MMP)2, MMP9, and proliferation-related protein Cyclin D1. Downregulation of CEP55 had the reverse effect. Moreover, the nuclear factor κB (NF-κB)/IκBα signalling pathway, which was activated in CEP55-transduced PANC cells and inhibited in CEP55-silenced PANC cells, contributed to CEP55-mediated PANC cell aggressiveness. This study provided new insights into the oncogenic roles of CEP55 and the mechanism by which the NF-κB pathway is hyperactivated in patients with PANC, indicating that CEP55 is a valuable prognostic factor and a potential therapeutic target in PANC.Tao PengWei ZhouFeng GuoHe-shui WuChun-you WangLi WangZhi-yong YangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tao Peng Wei Zhou Feng Guo He-shui Wu Chun-you Wang Li Wang Zhi-yong Yang Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
description	Abstract Centrosomal protein 55 (CEP55) is a microtubule-bundling protein that participants in cell mitosis. It is overexpressed in several solid tumours and promotes the growth and invasion of cancer cells. However, the role of CEP55 in pancreatic cancer (PANC) remains unclear. Herein, upregulated expression of CEP55 (associated with poor prognosis) was detected in PANC using quantitative real-time reverse transcription PCR, western blotting, and immunohistochemistry. Cell migration, colony formation, wound-healing, and Transwell matrix penetration assays, revealed that upregulation of CEP55 promoted PANC cells proliferation, migration, and invasion in vitro, whereas knockdown of CEP55 attenuated it. In an in vivo murine model, CEP55 overexpression accelerated PANC cells tumourigenicity, together with upregulation of the protein levels of invasion-related proteins matrix metalloproteinase (MMP)2, MMP9, and proliferation-related protein Cyclin D1. Downregulation of CEP55 had the reverse effect. Moreover, the nuclear factor κB (NF-κB)/IκBα signalling pathway, which was activated in CEP55-transduced PANC cells and inhibited in CEP55-silenced PANC cells, contributed to CEP55-mediated PANC cell aggressiveness. This study provided new insights into the oncogenic roles of CEP55 and the mechanism by which the NF-κB pathway is hyperactivated in patients with PANC, indicating that CEP55 is a valuable prognostic factor and a potential therapeutic target in PANC.
format	article
author	Tao Peng Wei Zhou Feng Guo He-shui Wu Chun-you Wang Li Wang Zhi-yong Yang
author_facet	Tao Peng Wei Zhou Feng Guo He-shui Wu Chun-you Wang Li Wang Zhi-yong Yang
author_sort	Tao Peng
title	Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
title_short	Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
title_full	Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
title_fullStr	Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
title_full_unstemmed	Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness
title_sort	centrosomal protein 55 activates nf-κb signalling and promotes pancreatic cancer cells aggressiveness
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/8617f4b80f9240a28f206e041b2c95f0
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Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

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