CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1

Abstract Tumor metastasis remains an obstacle in cancer treatment and is responsible for most cancer-related deaths. Nm23-H1 is one of the first metastasis suppressor proteins discovered with the ability to inhibit metastasis of many cancers including breast, colon, and liver cancer. Although loss o...

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Autores principales:	Ka Ming Wong, Jiaxing Song, Yung H. Wong
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d49a52eb047a4244bf60731c7eda808e
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spelling	oai:doaj.org-article:d49a52eb047a4244bf60731c7eda808e2021-12-02T14:12:45ZCTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H110.1038/s41598-020-79869-92045-2322https://doaj.org/article/d49a52eb047a4244bf60731c7eda808e2021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-79869-9https://doaj.org/toc/2045-2322Abstract Tumor metastasis remains an obstacle in cancer treatment and is responsible for most cancer-related deaths. Nm23-H1 is one of the first metastasis suppressor proteins discovered with the ability to inhibit metastasis of many cancers including breast, colon, and liver cancer. Although loss of Nm23-H1 is observed in aggressive cancers and correlated with metastatic potential, little is known regarding the mechanisms that regulate its cellular level. Here, we examined the mechanisms that control Nm23-H1 expression in breast cancer cells. Initial studies in aggressive MDA-MB-231 cells (expressing low Nm23-H1) and less invasive MCF-7 cells (expressing high Nm23-H1) revealed that mRNA levels correlated with protein expression, suggesting that transcriptional mechanisms may control Nm23-H1 expression. Truncational analysis of the Nm23-H1 promoter revealed a proximal and minimal promoter that harbor putative binding sites for transcription factors including CTCF and EGR1. CTCF and EGR1 induced Nm23-H1 expression and reduced cell migration of MDA-MB-231 cells. Moreover, CTCF and EGR1 were recruited to the Nm23-H1 promoter in MCF-7 cells and their expression correlated with Nm23-H1 levels. This study indicates that loss of Nm23-H1 in aggressive breast cancer is apparently caused by downregulation of CTCF and EGR1, which potentially drive Nm23-H1 expression to promote a less invasive phenotype.Ka Ming WongJiaxing SongYung H. WongNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-18 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ka Ming Wong Jiaxing Song Yung H. Wong CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
description	Abstract Tumor metastasis remains an obstacle in cancer treatment and is responsible for most cancer-related deaths. Nm23-H1 is one of the first metastasis suppressor proteins discovered with the ability to inhibit metastasis of many cancers including breast, colon, and liver cancer. Although loss of Nm23-H1 is observed in aggressive cancers and correlated with metastatic potential, little is known regarding the mechanisms that regulate its cellular level. Here, we examined the mechanisms that control Nm23-H1 expression in breast cancer cells. Initial studies in aggressive MDA-MB-231 cells (expressing low Nm23-H1) and less invasive MCF-7 cells (expressing high Nm23-H1) revealed that mRNA levels correlated with protein expression, suggesting that transcriptional mechanisms may control Nm23-H1 expression. Truncational analysis of the Nm23-H1 promoter revealed a proximal and minimal promoter that harbor putative binding sites for transcription factors including CTCF and EGR1. CTCF and EGR1 induced Nm23-H1 expression and reduced cell migration of MDA-MB-231 cells. Moreover, CTCF and EGR1 were recruited to the Nm23-H1 promoter in MCF-7 cells and their expression correlated with Nm23-H1 levels. This study indicates that loss of Nm23-H1 in aggressive breast cancer is apparently caused by downregulation of CTCF and EGR1, which potentially drive Nm23-H1 expression to promote a less invasive phenotype.
format	article
author	Ka Ming Wong Jiaxing Song Yung H. Wong
author_facet	Ka Ming Wong Jiaxing Song Yung H. Wong
author_sort	Ka Ming Wong
title	CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
title_short	CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
title_full	CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
title_fullStr	CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
title_full_unstemmed	CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1
title_sort	ctcf and egr1 suppress breast cancer cell migration through transcriptional control of nm23-h1
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/d49a52eb047a4244bf60731c7eda808e
work_keys_str_mv	AT kamingwong ctcfandegr1suppressbreastcancercellmigrationthroughtranscriptionalcontrolofnm23h1 AT jiaxingsong ctcfandegr1suppressbreastcancercellmigrationthroughtranscriptionalcontrolofnm23h1 AT yunghwong ctcfandegr1suppressbreastcancercellmigrationthroughtranscriptionalcontrolofnm23h1
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CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1

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