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Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9

Colorectal cancer (CRC) has been one of the most common types of cancer for decades worldwide. The pathogenesis of CRC is associated with the processes of activating oncogenes and inactivating anti-oncogenes. Platelet-derived growth factor-D (PDGF-D) was confirmed to regulate migration, invasion, pr...

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Autores principales: Jiang, Bin, Chen, Jinhuang, Yuan, Wenzheng, Ji, Jintong, Liu, Zhengyi, Wu, Liang, Tang, Qiang, Shu, Xiaogang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5777126/
https://www.ncbi.nlm.nih.gov/pubmed/29434852
http://dx.doi.org/10.3892/ol.2017.7510
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author Jiang, Bin
Chen, Jinhuang
Yuan, Wenzheng
Ji, Jintong
Liu, Zhengyi
Wu, Liang
Tang, Qiang
Shu, Xiaogang
author_facet Jiang, Bin
Chen, Jinhuang
Yuan, Wenzheng
Ji, Jintong
Liu, Zhengyi
Wu, Liang
Tang, Qiang
Shu, Xiaogang
author_sort Jiang, Bin
collection PubMed
description Colorectal cancer (CRC) has been one of the most common types of cancer for decades worldwide. The pathogenesis of CRC is associated with the processes of activating oncogenes and inactivating anti-oncogenes. Platelet-derived growth factor-D (PDGF-D) was confirmed to regulate migration, invasion, proliferation, apoptosis and metastasis in various cancer cells. Overexpression of PDGF-D exists in a number of human malignancies, including pancreatic, prostate and breast cancer. However, the expression and function of PDGF-D and its associated molecular mechanism in CRC remain unclear. Thus, the expression of PDGF-D was detected in CRC tissues and human colon cancer lines. Subsequently, the effects of PDGF-D on the invasion, migration and proliferation of cancer cells were investigated. The corresponding molecular mechanism had also been explored. The present study revealed that PDGF-D was upregulated not only in CRC tissues but also in CRC cell lines, and simultaneously, facilitated the processes of migration, invasion and proliferation. Silencing PDGF-D in the SW480 cell line inhibited migration, invasion and proliferation distinctly, with reduced expression of Notch1 and matrix metalloproteinase-9. Furthermore, upregulating PDGF-D in HCT116 cells led to the opposite results. These findings indicate that PDGF-D may be developed into a potential therapeutic target for CRC treatment.
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spelling pubmed-57771262018-02-12 Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9 Jiang, Bin Chen, Jinhuang Yuan, Wenzheng Ji, Jintong Liu, Zhengyi Wu, Liang Tang, Qiang Shu, Xiaogang Oncol Lett Articles Colorectal cancer (CRC) has been one of the most common types of cancer for decades worldwide. The pathogenesis of CRC is associated with the processes of activating oncogenes and inactivating anti-oncogenes. Platelet-derived growth factor-D (PDGF-D) was confirmed to regulate migration, invasion, proliferation, apoptosis and metastasis in various cancer cells. Overexpression of PDGF-D exists in a number of human malignancies, including pancreatic, prostate and breast cancer. However, the expression and function of PDGF-D and its associated molecular mechanism in CRC remain unclear. Thus, the expression of PDGF-D was detected in CRC tissues and human colon cancer lines. Subsequently, the effects of PDGF-D on the invasion, migration and proliferation of cancer cells were investigated. The corresponding molecular mechanism had also been explored. The present study revealed that PDGF-D was upregulated not only in CRC tissues but also in CRC cell lines, and simultaneously, facilitated the processes of migration, invasion and proliferation. Silencing PDGF-D in the SW480 cell line inhibited migration, invasion and proliferation distinctly, with reduced expression of Notch1 and matrix metalloproteinase-9. Furthermore, upregulating PDGF-D in HCT116 cells led to the opposite results. These findings indicate that PDGF-D may be developed into a potential therapeutic target for CRC treatment. D.A. Spandidos 2018-02 2017-12-05 /pmc/articles/PMC5777126/ /pubmed/29434852 http://dx.doi.org/10.3892/ol.2017.7510 Text en Copyright: © Jiang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Jiang, Bin
Chen, Jinhuang
Yuan, Wenzheng
Ji, Jintong
Liu, Zhengyi
Wu, Liang
Tang, Qiang
Shu, Xiaogang
Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title_full Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title_fullStr Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title_full_unstemmed Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title_short Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9
title_sort platelet-derived growth factor-d promotes colorectal cancer cell migration, invasion and proliferation by regulating notch1 and matrix metalloproteinase-9
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5777126/
https://www.ncbi.nlm.nih.gov/pubmed/29434852
http://dx.doi.org/10.3892/ol.2017.7510
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