AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.

Epithelial Mesenchymal Transition (EMT) plays a major role in cancer metastasis. Several genes have been shown to play a role in EMT, and one of these is Amplified-in-breast cancer 1 (AIB1), which has oncogenic function and is known to be amplified in breast cancer. However, the role of AIB1 in EMT...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Miao Wang, Feng Zhao, Shujing Li, Alan K Chang, Zhaojun Jia, Yixuan Chen, Feihong Xu, Hongming Pan, Huijian Wu
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a9c23c38cf304d12bf62d0fe1febb3af
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:a9c23c38cf304d12bf62d0fe1febb3af
record_format	dspace
spelling	oai:doaj.org-article:a9c23c38cf304d12bf62d0fe1febb3af2021-11-18T07:42:35ZAIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.1932-620310.1371/journal.pone.0065556https://doaj.org/article/a9c23c38cf304d12bf62d0fe1febb3af2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23762395/?tool=EBIhttps://doaj.org/toc/1932-6203Epithelial Mesenchymal Transition (EMT) plays a major role in cancer metastasis. Several genes have been shown to play a role in EMT, and one of these is Amplified-in-breast cancer 1 (AIB1), which has oncogenic function and is known to be amplified in breast cancer. However, the role of AIB1 in EMT remains largely undefined at the molecular level. In this study, the effect of AIB1 overexpression on the EMT of the breast cancer cell line T47D was investigated. Overexpression of AIB1 disrupted the epithelial morphology of the cells. At the same time, the cells displayed a strong metastasis and reduced level of the epithelial marker E-cadherin. In contrast, knockdown of AIB1 in T47D cells increased cell-cell adhesion and produced weak metastasis, as well as a higher level of E-cadherin expression. We proposed that the regulation of EMT by AIB1 occurred through the action of the transcription factor SNAI1, and demonstrated that such interaction required the participation of ERα and the presence of ERα-binding site on SNAI1 promoter. The expression level of E-cadherin and the extent of cell migration and invasion in SNAI1-knocked down T47D cells that overexpressed AIB1 were similar to those of T47D cells that did not overexpress AIB1 and had no SNAI1 knockdown. Taken together, these results suggested that AIB1 exerted its effect on EMT through its interaction with ERα, which could directly bind to the ERα-binding site on the SNAI1 promoter, allowing the AIB1-ERα complex to promote the transcription of SNAI1 and eventually led to repression of E-cadherin expression, consistent with the loss of E-cadherin being a hallmark of EMT.Miao WangFeng ZhaoShujing LiAlan K ChangZhaojun JiaYixuan ChenFeihong XuHongming PanHuijian WuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e65556 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Miao Wang Feng Zhao Shujing Li Alan K Chang Zhaojun Jia Yixuan Chen Feihong Xu Hongming Pan Huijian Wu AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
description	Epithelial Mesenchymal Transition (EMT) plays a major role in cancer metastasis. Several genes have been shown to play a role in EMT, and one of these is Amplified-in-breast cancer 1 (AIB1), which has oncogenic function and is known to be amplified in breast cancer. However, the role of AIB1 in EMT remains largely undefined at the molecular level. In this study, the effect of AIB1 overexpression on the EMT of the breast cancer cell line T47D was investigated. Overexpression of AIB1 disrupted the epithelial morphology of the cells. At the same time, the cells displayed a strong metastasis and reduced level of the epithelial marker E-cadherin. In contrast, knockdown of AIB1 in T47D cells increased cell-cell adhesion and produced weak metastasis, as well as a higher level of E-cadherin expression. We proposed that the regulation of EMT by AIB1 occurred through the action of the transcription factor SNAI1, and demonstrated that such interaction required the participation of ERα and the presence of ERα-binding site on SNAI1 promoter. The expression level of E-cadherin and the extent of cell migration and invasion in SNAI1-knocked down T47D cells that overexpressed AIB1 were similar to those of T47D cells that did not overexpress AIB1 and had no SNAI1 knockdown. Taken together, these results suggested that AIB1 exerted its effect on EMT through its interaction with ERα, which could directly bind to the ERα-binding site on the SNAI1 promoter, allowing the AIB1-ERα complex to promote the transcription of SNAI1 and eventually led to repression of E-cadherin expression, consistent with the loss of E-cadherin being a hallmark of EMT.
format	article
author	Miao Wang Feng Zhao Shujing Li Alan K Chang Zhaojun Jia Yixuan Chen Feihong Xu Hongming Pan Huijian Wu
author_facet	Miao Wang Feng Zhao Shujing Li Alan K Chang Zhaojun Jia Yixuan Chen Feihong Xu Hongming Pan Huijian Wu
author_sort	Miao Wang
title	AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
title_short	AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
title_full	AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
title_fullStr	AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
title_full_unstemmed	AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.
title_sort	aib1 cooperates with erα to promote epithelial mesenchymal transition in breast cancer through snai1 activation.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/a9c23c38cf304d12bf62d0fe1febb3af
work_keys_str_mv	AT miaowang aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT fengzhao aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT shujingli aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT alankchang aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT zhaojunjia aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT yixuanchen aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT feihongxu aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT hongmingpan aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation AT huijianwu aib1cooperateswitheratopromoteepithelialmesenchymaltransitioninbreastcancerthroughsnai1activation
_version_	1718423118540701696

AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.

Ejemplares similares