RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer

Abstract RUFY3 is highly expressed in brain tissue and has a role in neuronal development. Transcriptional factor FOXK1 is involved in cell growth and metabolism. We knew that RUFY3 or FOXK1 has been correlated with the malignant of tumor cells. However, the role of these molecules in colorectal can...

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Autores principales:	Ruyi Xie, Jing Wang, Xuehua Liu, Liqing Wu, Hui Zhang, Weimei Tang, Yueqiao Li, Li Xiang, Ying Peng, Xiaoting Huang, Yang Bai, Guangnan Liu, Aimin Li, Yadong Wang, Ye Chen, Yuexin Ren, Guoxin Li, Wei Gong, Side Liu, Jide Wang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bfde73ef2cb7474aa67630f6c01fe7f9
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spelling	oai:doaj.org-article:bfde73ef2cb7474aa67630f6c01fe7f92021-12-02T12:32:43ZRUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer10.1038/s41598-017-04011-12045-2322https://doaj.org/article/bfde73ef2cb7474aa67630f6c01fe7f92017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04011-1https://doaj.org/toc/2045-2322Abstract RUFY3 is highly expressed in brain tissue and has a role in neuronal development. Transcriptional factor FOXK1 is involved in cell growth and metabolism. We knew that RUFY3 or FOXK1 has been correlated with the malignant of tumor cells. However, the role of these molecules in colorectal cancer (CRC) progression remains unknown. We investigated the protein expression levels by Western blot, immunofluorescence and immunohistochemistry analyses. The migration and invasive abilities of CRC cells were assessed using shRNA-mediated inhibition in vitro and in vivo. We showed that RUFY3 expression was up-regulated in CRC compared with its expression in a normal human colon cell line (FHC). RUFY3 suppression inhibited anchorage independent cell tumorigenesis. RUFY3 induced elevated expression of eight major oncogenes. Moreover, RUFY3 physically interacts with FOXK1 in CRC. A positive correlation was observed between the expression patterns of RUFY3 and FOXK1. Furthermore, RUFY3 and FOXK1 expression were correlated with tumor progression and represented significant predictors of overall survival in CRC patients. SiRNA-mediated repression of FOXK1 in RUFY3-overexpressing cells reversed the epithelial-mesenchymal transition (EMT) and metastatic phenotypes. In vivo, FOXK1 promoted RUFY3-mediated metastasis via orthotopic implantation. These findings suggest that the RUFY3-FOXK1 axis might promote the development and progression of human CRC.Ruyi XieJing WangXuehua LiuLiqing WuHui ZhangWeimei TangYueqiao LiLi XiangYing PengXiaoting HuangYang BaiGuangnan LiuAimin LiYadong WangYe ChenYuexin RenGuoxin LiWei GongSide LiuJide WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ruyi Xie Jing Wang Xuehua Liu Liqing Wu Hui Zhang Weimei Tang Yueqiao Li Li Xiang Ying Peng Xiaoting Huang Yang Bai Guangnan Liu Aimin Li Yadong Wang Ye Chen Yuexin Ren Guoxin Li Wei Gong Side Liu Jide Wang RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
description	Abstract RUFY3 is highly expressed in brain tissue and has a role in neuronal development. Transcriptional factor FOXK1 is involved in cell growth and metabolism. We knew that RUFY3 or FOXK1 has been correlated with the malignant of tumor cells. However, the role of these molecules in colorectal cancer (CRC) progression remains unknown. We investigated the protein expression levels by Western blot, immunofluorescence and immunohistochemistry analyses. The migration and invasive abilities of CRC cells were assessed using shRNA-mediated inhibition in vitro and in vivo. We showed that RUFY3 expression was up-regulated in CRC compared with its expression in a normal human colon cell line (FHC). RUFY3 suppression inhibited anchorage independent cell tumorigenesis. RUFY3 induced elevated expression of eight major oncogenes. Moreover, RUFY3 physically interacts with FOXK1 in CRC. A positive correlation was observed between the expression patterns of RUFY3 and FOXK1. Furthermore, RUFY3 and FOXK1 expression were correlated with tumor progression and represented significant predictors of overall survival in CRC patients. SiRNA-mediated repression of FOXK1 in RUFY3-overexpressing cells reversed the epithelial-mesenchymal transition (EMT) and metastatic phenotypes. In vivo, FOXK1 promoted RUFY3-mediated metastasis via orthotopic implantation. These findings suggest that the RUFY3-FOXK1 axis might promote the development and progression of human CRC.
format	article
author	Ruyi Xie Jing Wang Xuehua Liu Liqing Wu Hui Zhang Weimei Tang Yueqiao Li Li Xiang Ying Peng Xiaoting Huang Yang Bai Guangnan Liu Aimin Li Yadong Wang Ye Chen Yuexin Ren Guoxin Li Wei Gong Side Liu Jide Wang
author_facet	Ruyi Xie Jing Wang Xuehua Liu Liqing Wu Hui Zhang Weimei Tang Yueqiao Li Li Xiang Ying Peng Xiaoting Huang Yang Bai Guangnan Liu Aimin Li Yadong Wang Ye Chen Yuexin Ren Guoxin Li Wei Gong Side Liu Jide Wang
author_sort	Ruyi Xie
title	RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
title_short	RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
title_full	RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
title_fullStr	RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
title_full_unstemmed	RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer
title_sort	rufy3 interaction with foxk1 promotes invasion and metastasis in colorectal cancer
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/bfde73ef2cb7474aa67630f6c01fe7f9
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RUFY3 interaction with FOXK1 promotes invasion and metastasis in colorectal cancer

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