DACH1 suppresses breast cancer as a negative regulator of CD44

Abstract Dachshund homolog 1 (DACH1), a key cell fate determination factor, contributes to tumorigenesis, invasion, metastasis of human breast neoplasm. However, the exact molecular mechanisms for the anti-tumor roles of DACH1 in breast carcinoma are still lack of extensive understanding. Herein, we...

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Autores principales:	Hanxiao Xu, Shengnan Yu, Xun Yuan, Jing Xiong, Dong Kuang, Richard G. Pestell, Kongming Wu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e163e6be23294792b97c2074697e192f
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spelling	oai:doaj.org-article:e163e6be23294792b97c2074697e192f2021-12-02T12:32:28ZDACH1 suppresses breast cancer as a negative regulator of CD4410.1038/s41598-017-04709-22045-2322https://doaj.org/article/e163e6be23294792b97c2074697e192f2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04709-2https://doaj.org/toc/2045-2322Abstract Dachshund homolog 1 (DACH1), a key cell fate determination factor, contributes to tumorigenesis, invasion, metastasis of human breast neoplasm. However, the exact molecular mechanisms for the anti-tumor roles of DACH1 in breast carcinoma are still lack of extensive understanding. Herein, we utilized immunohistochemistry (IHC) staining and public microarray data analysis showing that DACH1 was higher in normal breast, low-grade and luminal-type cancer in comparison with breast carcinoma, high-grade and basal-like tumors respectively. Additionally, both correlation analysis of public databases of human breast carcinoma and IHC analysis of mice xenograft tumors demonstrated that DACH1 inversely related to cancer stem cells (CSCs) markers, epithelial-mesenchymal transition (EMT) inducers and basal-enriched molecules, while cluster of differentiation 44 (CD44) behaved in an opposite manner. Furthermore, mice transplanted tumor model indicated that breast cancer cells Met-1 with up-regulation of DACH1 were endowed with remarkably reduced potential of tumorigenesis. Importantly, meta-analysis of 19 Gene Expression Omnibus (GEO) databases of breast cancer implicated that patients with higher DACH1 expression had prolonged time to death, recurrence and metastasis, while CD44 was a promising biomarker predicting worse overall survival (OS) and metastasis-free survival (MFS). Collectively, our study indicated that CD44 might be a novel target of DACH1 in breast carcinoma.Hanxiao XuShengnan YuXun YuanJing XiongDong KuangRichard G. PestellKongming WuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hanxiao Xu Shengnan Yu Xun Yuan Jing Xiong Dong Kuang Richard G. Pestell Kongming Wu DACH1 suppresses breast cancer as a negative regulator of CD44
description	Abstract Dachshund homolog 1 (DACH1), a key cell fate determination factor, contributes to tumorigenesis, invasion, metastasis of human breast neoplasm. However, the exact molecular mechanisms for the anti-tumor roles of DACH1 in breast carcinoma are still lack of extensive understanding. Herein, we utilized immunohistochemistry (IHC) staining and public microarray data analysis showing that DACH1 was higher in normal breast, low-grade and luminal-type cancer in comparison with breast carcinoma, high-grade and basal-like tumors respectively. Additionally, both correlation analysis of public databases of human breast carcinoma and IHC analysis of mice xenograft tumors demonstrated that DACH1 inversely related to cancer stem cells (CSCs) markers, epithelial-mesenchymal transition (EMT) inducers and basal-enriched molecules, while cluster of differentiation 44 (CD44) behaved in an opposite manner. Furthermore, mice transplanted tumor model indicated that breast cancer cells Met-1 with up-regulation of DACH1 were endowed with remarkably reduced potential of tumorigenesis. Importantly, meta-analysis of 19 Gene Expression Omnibus (GEO) databases of breast cancer implicated that patients with higher DACH1 expression had prolonged time to death, recurrence and metastasis, while CD44 was a promising biomarker predicting worse overall survival (OS) and metastasis-free survival (MFS). Collectively, our study indicated that CD44 might be a novel target of DACH1 in breast carcinoma.
format	article
author	Hanxiao Xu Shengnan Yu Xun Yuan Jing Xiong Dong Kuang Richard G. Pestell Kongming Wu
author_facet	Hanxiao Xu Shengnan Yu Xun Yuan Jing Xiong Dong Kuang Richard G. Pestell Kongming Wu
author_sort	Hanxiao Xu
title	DACH1 suppresses breast cancer as a negative regulator of CD44
title_short	DACH1 suppresses breast cancer as a negative regulator of CD44
title_full	DACH1 suppresses breast cancer as a negative regulator of CD44
title_fullStr	DACH1 suppresses breast cancer as a negative regulator of CD44
title_full_unstemmed	DACH1 suppresses breast cancer as a negative regulator of CD44
title_sort	dach1 suppresses breast cancer as a negative regulator of cd44
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/e163e6be23294792b97c2074697e192f
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_version_	1718394068875083776

DACH1 suppresses breast cancer as a negative regulator of CD44

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