Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth

Abstract Angiogenesis is a physiological process for the formation of new blood vessels from the pre-existing vessels and it has a vital role in the survival and growth of neoplasms. During tumor angiogenesis, the activation of the gene transcriptions in vascular endothelial cells (ECs) plays an ess...

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Autores principales:	Huan Liu, Yikai Qiu, Xiuying Pei, Ramamurthy Chitteti, Rebbeca Steiner, Shuya Zhang, Zheng Gen Jin
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9c4a57dd2aa34930a02d3214c650fdc3
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spelling	oai:doaj.org-article:9c4a57dd2aa34930a02d3214c650fdc32021-12-02T15:10:19ZEndothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth10.1038/s41598-020-77568-z2045-2322https://doaj.org/article/9c4a57dd2aa34930a02d3214c650fdc32020-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-77568-zhttps://doaj.org/toc/2045-2322Abstract Angiogenesis is a physiological process for the formation of new blood vessels from the pre-existing vessels and it has a vital role in the survival and growth of neoplasms. During tumor angiogenesis, the activation of the gene transcriptions in vascular endothelial cells (ECs) plays an essential role in the promotion of EC proliferation, migration, and vascular network development. However, the molecular mechanisms underlying transcriptional regulation of EC and tumor angiogenesis remains to be fully elucidated. Here we report that the transcription factor Yin Yang 1 (YY1) in ECs is critically involved in tumor angiogenesis. First, we utilized a tamoxifen-inducible EC-specific YY1 deficient mouse model and showed that YY1 deletion in ECs inhibited the tumor growth and tumor angiogenesis. Using the in vivo matrigel plug assay, we then found that EC-specific YY1 ablation inhibited growth factor-induced angiogenesis. Furthermore, vascular endothelial growth factor (VEGF)-induced EC migration was diminished in YY1-depleted human umbilical vein endothelial cells (HUVECs). Finally, a rescue experiment revealed that YY1-regulated BMP6 expression in ECs was involved in EC migration. Collectively, our results demonstrate that endothelial YY1 has a crucial role in tumor angiogenesis and suggest that targeting endothelial YY1 could be a potential therapeutic strategy for cancer treatment.Huan LiuYikai QiuXiuying PeiRamamurthy ChittetiRebbeca SteinerShuya ZhangZheng Gen JinNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-11 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Huan Liu Yikai Qiu Xiuying Pei Ramamurthy Chitteti Rebbeca Steiner Shuya Zhang Zheng Gen Jin Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
description	Abstract Angiogenesis is a physiological process for the formation of new blood vessels from the pre-existing vessels and it has a vital role in the survival and growth of neoplasms. During tumor angiogenesis, the activation of the gene transcriptions in vascular endothelial cells (ECs) plays an essential role in the promotion of EC proliferation, migration, and vascular network development. However, the molecular mechanisms underlying transcriptional regulation of EC and tumor angiogenesis remains to be fully elucidated. Here we report that the transcription factor Yin Yang 1 (YY1) in ECs is critically involved in tumor angiogenesis. First, we utilized a tamoxifen-inducible EC-specific YY1 deficient mouse model and showed that YY1 deletion in ECs inhibited the tumor growth and tumor angiogenesis. Using the in vivo matrigel plug assay, we then found that EC-specific YY1 ablation inhibited growth factor-induced angiogenesis. Furthermore, vascular endothelial growth factor (VEGF)-induced EC migration was diminished in YY1-depleted human umbilical vein endothelial cells (HUVECs). Finally, a rescue experiment revealed that YY1-regulated BMP6 expression in ECs was involved in EC migration. Collectively, our results demonstrate that endothelial YY1 has a crucial role in tumor angiogenesis and suggest that targeting endothelial YY1 could be a potential therapeutic strategy for cancer treatment.
format	article
author	Huan Liu Yikai Qiu Xiuying Pei Ramamurthy Chitteti Rebbeca Steiner Shuya Zhang Zheng Gen Jin
author_facet	Huan Liu Yikai Qiu Xiuying Pei Ramamurthy Chitteti Rebbeca Steiner Shuya Zhang Zheng Gen Jin
author_sort	Huan Liu
title	Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
title_short	Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
title_full	Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
title_fullStr	Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
title_full_unstemmed	Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth
title_sort	endothelial specific yy1 deletion restricts tumor angiogenesis and tumor growth
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/9c4a57dd2aa34930a02d3214c650fdc3
work_keys_str_mv	AT huanliu endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT yikaiqiu endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT xiuyingpei endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT ramamurthychitteti endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT rebbecasteiner endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT shuyazhang endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth AT zhenggenjin endothelialspecificyy1deletionrestrictstumorangiogenesisandtumorgrowth
_version_	1718387707748548608

Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth

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