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Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition
Transcriptional factor FOXK1 is a member of the FOX family, involved in the cell growth and metabolism. The higher expression of FOXK1 leads to a variety of diseases and may play an important role in the development of various tumors. However, the role of FOXK1 in the progression of colorectal cance...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5239465/ https://www.ncbi.nlm.nih.gov/pubmed/27223064 http://dx.doi.org/10.18632/oncotarget.9457 |
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author | Wu, Yao Peng, Ying Wu, Meiyan Zhang, Wenjing Zhang, Mengnan Xie, Ruyi Zhang, Pei Bai, Yang Zhao, Jinjun Li, Aimin Nan, Qingzhen Chen, Ye Ren, Yuexin Liu, Side Wang, Jide |
author_facet | Wu, Yao Peng, Ying Wu, Meiyan Zhang, Wenjing Zhang, Mengnan Xie, Ruyi Zhang, Pei Bai, Yang Zhao, Jinjun Li, Aimin Nan, Qingzhen Chen, Ye Ren, Yuexin Liu, Side Wang, Jide |
author_sort | Wu, Yao |
collection | PubMed |
description | Transcriptional factor FOXK1 is a member of the FOX family, involved in the cell growth and metabolism. The higher expression of FOXK1 leads to a variety of diseases and may play an important role in the development of various tumors. However, the role of FOXK1 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that FOXK1 was overexpressed in 16 types of solid tumor tissues via tissue multi-array (TMA). We found that FOXK1 induced elevated expressions and transactivities of five major oncogenes in CRC. Moreover, the elevated expression of FOXK1 was showed to be correlated with tumor progression and was a significant predictor of overall survival in CRC patients. Furthermore, it was showed that the depletion of FOXK1 expression could inhibit the migratory and invasive abilities of CRC cells. In contrast, ectopic expression of FOXK1 elicited the opposite effects on these phenotypes in vitro. FOXK1 promoted tumor metastasis through EMT program induction. In addition, TGF-β1 induced FOXK1 expression in a time-dependent pattern and the knockdown of FOXK1 inhibited TGF-β1-induced EMT. In vivo, higher expression of FOXK1 promotes CRC cell invasion and metastasis, and induces EMT in CRC as well. Alltogether, it was concluded that the higher expression of FOXK1 could indicate a poor prognosis in CRC patients since that FOXK1 induces EMT and promotes CRC cell invasion in vitro and in vivo. |
format | Online Article Text |
id | pubmed-5239465 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-52394652017-01-24 Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition Wu, Yao Peng, Ying Wu, Meiyan Zhang, Wenjing Zhang, Mengnan Xie, Ruyi Zhang, Pei Bai, Yang Zhao, Jinjun Li, Aimin Nan, Qingzhen Chen, Ye Ren, Yuexin Liu, Side Wang, Jide Oncotarget Research Paper Transcriptional factor FOXK1 is a member of the FOX family, involved in the cell growth and metabolism. The higher expression of FOXK1 leads to a variety of diseases and may play an important role in the development of various tumors. However, the role of FOXK1 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that FOXK1 was overexpressed in 16 types of solid tumor tissues via tissue multi-array (TMA). We found that FOXK1 induced elevated expressions and transactivities of five major oncogenes in CRC. Moreover, the elevated expression of FOXK1 was showed to be correlated with tumor progression and was a significant predictor of overall survival in CRC patients. Furthermore, it was showed that the depletion of FOXK1 expression could inhibit the migratory and invasive abilities of CRC cells. In contrast, ectopic expression of FOXK1 elicited the opposite effects on these phenotypes in vitro. FOXK1 promoted tumor metastasis through EMT program induction. In addition, TGF-β1 induced FOXK1 expression in a time-dependent pattern and the knockdown of FOXK1 inhibited TGF-β1-induced EMT. In vivo, higher expression of FOXK1 promotes CRC cell invasion and metastasis, and induces EMT in CRC as well. Alltogether, it was concluded that the higher expression of FOXK1 could indicate a poor prognosis in CRC patients since that FOXK1 induces EMT and promotes CRC cell invasion in vitro and in vivo. Impact Journals LLC 2016-05-19 /pmc/articles/PMC5239465/ /pubmed/27223064 http://dx.doi.org/10.18632/oncotarget.9457 Text en Copyright: © 2016 Wu et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Wu, Yao Peng, Ying Wu, Meiyan Zhang, Wenjing Zhang, Mengnan Xie, Ruyi Zhang, Pei Bai, Yang Zhao, Jinjun Li, Aimin Nan, Qingzhen Chen, Ye Ren, Yuexin Liu, Side Wang, Jide Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title | Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title_full | Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title_fullStr | Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title_full_unstemmed | Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title_short | Oncogene FOXK1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
title_sort | oncogene foxk1 enhances invasion of colorectal carcinoma by inducing epithelial-mesenchymal transition |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5239465/ https://www.ncbi.nlm.nih.gov/pubmed/27223064 http://dx.doi.org/10.18632/oncotarget.9457 |
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