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Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells
Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increase...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932528/ https://www.ncbi.nlm.nih.gov/pubmed/27377307 http://dx.doi.org/10.1038/srep29385 |
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author | Ying, Tsung-Ho Lee, Chien-Hsing Chiou, Hui-Ling Yang, Shun-Fa Lin, Chu-Liang Hung, Chia-Hung Tsai, Jen-Pi Hsieh, Yi-Hsien |
author_facet | Ying, Tsung-Ho Lee, Chien-Hsing Chiou, Hui-Ling Yang, Shun-Fa Lin, Chu-Liang Hung, Chia-Hung Tsai, Jen-Pi Hsieh, Yi-Hsien |
author_sort | Ying, Tsung-Ho |
collection | PubMed |
description | Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increased PTX3 expression was significantly associated with tumor grade (P < 0.011) and differentiation (P < 0.019). Knocking down PTX3 with lentivirus-mediated small hairpin RNA (shRNA) in cervical cancer cell lines resulted in inhibited cell viability, diminished colony-forming ability, and induced cell cycle arrest at the G2/M phase of the cell cycle, along with downregulated expression of cyclin B1, cdc2, and cdc25c, and upregulated expression of p-cdc2, p-cdc25c, p21, and p27. Furthermore, knockdown of PTX3 significantly decreased the potential of migration and invasion of cervical cancer cells by inhibiting matrix metalloproteidase-2 (MMP-2), MMP-9, and urokinase plasminogen activator (uPA). Moreover, in vivo functional studies showed PTX3-knockdown in mice suppressed tumorigenicity and lung metastatic potential. Conversely, overexpression of PTX3 enhanced proliferation and invasion both in vitro and in vivo. Our results demonstrated that PTX3 contributes to tumorigenesis and metastasis of human cervical cancer cells. Further studies are warranted to demonstrate PTX3 as a novel therapeutic biomarker for human cervical cancer. |
format | Online Article Text |
id | pubmed-4932528 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49325282016-07-08 Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells Ying, Tsung-Ho Lee, Chien-Hsing Chiou, Hui-Ling Yang, Shun-Fa Lin, Chu-Liang Hung, Chia-Hung Tsai, Jen-Pi Hsieh, Yi-Hsien Sci Rep Article Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increased PTX3 expression was significantly associated with tumor grade (P < 0.011) and differentiation (P < 0.019). Knocking down PTX3 with lentivirus-mediated small hairpin RNA (shRNA) in cervical cancer cell lines resulted in inhibited cell viability, diminished colony-forming ability, and induced cell cycle arrest at the G2/M phase of the cell cycle, along with downregulated expression of cyclin B1, cdc2, and cdc25c, and upregulated expression of p-cdc2, p-cdc25c, p21, and p27. Furthermore, knockdown of PTX3 significantly decreased the potential of migration and invasion of cervical cancer cells by inhibiting matrix metalloproteidase-2 (MMP-2), MMP-9, and urokinase plasminogen activator (uPA). Moreover, in vivo functional studies showed PTX3-knockdown in mice suppressed tumorigenicity and lung metastatic potential. Conversely, overexpression of PTX3 enhanced proliferation and invasion both in vitro and in vivo. Our results demonstrated that PTX3 contributes to tumorigenesis and metastasis of human cervical cancer cells. Further studies are warranted to demonstrate PTX3 as a novel therapeutic biomarker for human cervical cancer. Nature Publishing Group 2016-07-05 /pmc/articles/PMC4932528/ /pubmed/27377307 http://dx.doi.org/10.1038/srep29385 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Ying, Tsung-Ho Lee, Chien-Hsing Chiou, Hui-Ling Yang, Shun-Fa Lin, Chu-Liang Hung, Chia-Hung Tsai, Jen-Pi Hsieh, Yi-Hsien Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title | Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title_full | Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title_fullStr | Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title_full_unstemmed | Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title_short | Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
title_sort | knockdown of pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932528/ https://www.ncbi.nlm.nih.gov/pubmed/27377307 http://dx.doi.org/10.1038/srep29385 |
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