author_facet Wang, Hao‐fan
Wang, Sha‐sha
Zheng, Min
Dai, Lu‐ling
Wang, Ke
Gao, Xiao‐lei
Cao, Ming‐xin
Yu, Xiang‐hua
Pang, Xin
Zhang, Mei
Wu, Jing‐biao
Wu, Jia‐shun
Yang, Xiao
Tang, Ya‐jie
Chen, Yu
Tang, Ya‐ling
Liang, Xin‐hua
Wang, Hao‐fan
Wang, Sha‐sha
Zheng, Min
Dai, Lu‐ling
Wang, Ke
Gao, Xiao‐lei
Cao, Ming‐xin
Yu, Xiang‐hua
Pang, Xin
Zhang, Mei
Wu, Jing‐biao
Wu, Jia‐shun
Yang, Xiao
Tang, Ya‐jie
Chen, Yu
Tang, Ya‐ling
Liang, Xin‐hua
author Wang, Hao‐fan
Wang, Sha‐sha
Zheng, Min
Dai, Lu‐ling
Wang, Ke
Gao, Xiao‐lei
Cao, Ming‐xin
Yu, Xiang‐hua
Pang, Xin
Zhang, Mei
Wu, Jing‐biao
Wu, Jia‐shun
Yang, Xiao
Tang, Ya‐jie
Chen, Yu
Tang, Ya‐ling
Liang, Xin‐hua
spellingShingle Wang, Hao‐fan
Wang, Sha‐sha
Zheng, Min
Dai, Lu‐ling
Wang, Ke
Gao, Xiao‐lei
Cao, Ming‐xin
Yu, Xiang‐hua
Pang, Xin
Zhang, Mei
Wu, Jing‐biao
Wu, Jia‐shun
Yang, Xiao
Tang, Ya‐jie
Chen, Yu
Tang, Ya‐ling
Liang, Xin‐hua
Cell Proliferation
Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
Cell Biology
General Medicine
author_sort wang, hao‐fan
spelling Wang, Hao‐fan Wang, Sha‐sha Zheng, Min Dai, Lu‐ling Wang, Ke Gao, Xiao‐lei Cao, Ming‐xin Yu, Xiang‐hua Pang, Xin Zhang, Mei Wu, Jing‐biao Wu, Jia‐shun Yang, Xiao Tang, Ya‐jie Chen, Yu Tang, Ya‐ling Liang, Xin‐hua 0960-7722 1365-2184 Wiley Cell Biology General Medicine http://dx.doi.org/10.1111/cpr.12600 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>To investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Firstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT‐PCR were used to detect the effect of hypoxia on VE‐cadherin and VEGFA expression. And pro‐vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E‐cadherin, N‐cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF‐1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF‐1α level were analysed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Hypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE‐cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N‐cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E‐cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF‐1α expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>VEGFA played an important role in hypoxia‐induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.</jats:p></jats:sec> Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma Cell Proliferation
doi_str_mv 10.1111/cpr.12600
facet_avail Online
Free
finc_class_facet Biologie
format ElectronicArticle
fullrecord blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9jcHIuMTI2MDA
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9jcHIuMTI2MDA
institution DE-Gla1
DE-Zi4
DE-15
DE-Pl11
DE-Rs1
DE-105
DE-14
DE-Ch1
DE-L229
DE-D275
DE-Bn3
DE-Brt1
DE-Zwi2
DE-D161
imprint Wiley, 2019
imprint_str_mv Wiley, 2019
issn 0960-7722
1365-2184
issn_str_mv 0960-7722
1365-2184
language English
mega_collection Wiley (CrossRef)
match_str wang2019hypoxiapromotesvasculogenicmimicryformationbyvascularendothelialgrowthfactoramediatingepithelialmesenchymaltransitioninsalivaryadenoidcysticcarcinoma
publishDateSort 2019
publisher Wiley
recordtype ai
record_format ai
series Cell Proliferation
source_id 49
title Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_unstemmed Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_full Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_fullStr Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_full_unstemmed Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_short Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_sort hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor a mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
topic Cell Biology
General Medicine
url http://dx.doi.org/10.1111/cpr.12600
publishDate 2019
physical
description <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>To investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Firstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT‐PCR were used to detect the effect of hypoxia on VE‐cadherin and VEGFA expression. And pro‐vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E‐cadherin, N‐cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF‐1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF‐1α level were analysed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Hypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE‐cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N‐cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E‐cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF‐1α expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>VEGFA played an important role in hypoxia‐induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.</jats:p></jats:sec>
container_issue 3
container_start_page 0
container_title Cell Proliferation
container_volume 52
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
_version_ 1792342657331101698
geogr_code not assigned
last_indexed 2024-03-01T16:39:15.945Z
geogr_code_person not assigned
openURL url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Hypoxia+promotes+vasculogenic+mimicry+formation+by+vascular+endothelial+growth+factor+A+mediating+epithelial%E2%80%90mesenchymal+transition+in+salivary+adenoid+cystic+carcinoma&rft.date=2019-05-01&genre=article&issn=1365-2184&volume=52&issue=3&jtitle=Cell+Proliferation&atitle=Hypoxia+promotes+vasculogenic+mimicry+formation+by+vascular+endothelial+growth+factor+A+mediating+epithelial%E2%80%90mesenchymal+transition+in+salivary+adenoid+cystic+carcinoma&aulast=Liang&aufirst=Xin%E2%80%90hua&rft_id=info%3Adoi%2F10.1111%2Fcpr.12600&rft.language%5B0%5D=eng
SOLR
_version_ 1792342657331101698
author Wang, Hao‐fan, Wang, Sha‐sha, Zheng, Min, Dai, Lu‐ling, Wang, Ke, Gao, Xiao‐lei, Cao, Ming‐xin, Yu, Xiang‐hua, Pang, Xin, Zhang, Mei, Wu, Jing‐biao, Wu, Jia‐shun, Yang, Xiao, Tang, Ya‐jie, Chen, Yu, Tang, Ya‐ling, Liang, Xin‐hua
author_facet Wang, Hao‐fan, Wang, Sha‐sha, Zheng, Min, Dai, Lu‐ling, Wang, Ke, Gao, Xiao‐lei, Cao, Ming‐xin, Yu, Xiang‐hua, Pang, Xin, Zhang, Mei, Wu, Jing‐biao, Wu, Jia‐shun, Yang, Xiao, Tang, Ya‐jie, Chen, Yu, Tang, Ya‐ling, Liang, Xin‐hua, Wang, Hao‐fan, Wang, Sha‐sha, Zheng, Min, Dai, Lu‐ling, Wang, Ke, Gao, Xiao‐lei, Cao, Ming‐xin, Yu, Xiang‐hua, Pang, Xin, Zhang, Mei, Wu, Jing‐biao, Wu, Jia‐shun, Yang, Xiao, Tang, Ya‐jie, Chen, Yu, Tang, Ya‐ling, Liang, Xin‐hua
author_sort wang, hao‐fan
container_issue 3
container_start_page 0
container_title Cell Proliferation
container_volume 52
description <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>To investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Firstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT‐PCR were used to detect the effect of hypoxia on VE‐cadherin and VEGFA expression. And pro‐vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E‐cadherin, N‐cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF‐1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF‐1α level were analysed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Hypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE‐cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N‐cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E‐cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF‐1α expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>VEGFA played an important role in hypoxia‐induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.</jats:p></jats:sec>
doi_str_mv 10.1111/cpr.12600
facet_avail Online, Free
finc_class_facet Biologie
format ElectronicArticle
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
geogr_code not assigned
geogr_code_person not assigned
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9jcHIuMTI2MDA
imprint Wiley, 2019
imprint_str_mv Wiley, 2019
institution DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161
issn 0960-7722, 1365-2184
issn_str_mv 0960-7722, 1365-2184
language English
last_indexed 2024-03-01T16:39:15.945Z
match_str wang2019hypoxiapromotesvasculogenicmimicryformationbyvascularendothelialgrowthfactoramediatingepithelialmesenchymaltransitioninsalivaryadenoidcysticcarcinoma
mega_collection Wiley (CrossRef)
physical
publishDate 2019
publishDateSort 2019
publisher Wiley
record_format ai
recordtype ai
series Cell Proliferation
source_id 49
spelling Wang, Hao‐fan Wang, Sha‐sha Zheng, Min Dai, Lu‐ling Wang, Ke Gao, Xiao‐lei Cao, Ming‐xin Yu, Xiang‐hua Pang, Xin Zhang, Mei Wu, Jing‐biao Wu, Jia‐shun Yang, Xiao Tang, Ya‐jie Chen, Yu Tang, Ya‐ling Liang, Xin‐hua 0960-7722 1365-2184 Wiley Cell Biology General Medicine http://dx.doi.org/10.1111/cpr.12600 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>To investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Firstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT‐PCR were used to detect the effect of hypoxia on VE‐cadherin and VEGFA expression. And pro‐vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E‐cadherin, N‐cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF‐1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF‐1α level were analysed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Hypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE‐cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N‐cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E‐cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF‐1α expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>VEGFA played an important role in hypoxia‐induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.</jats:p></jats:sec> Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma Cell Proliferation
spellingShingle Wang, Hao‐fan, Wang, Sha‐sha, Zheng, Min, Dai, Lu‐ling, Wang, Ke, Gao, Xiao‐lei, Cao, Ming‐xin, Yu, Xiang‐hua, Pang, Xin, Zhang, Mei, Wu, Jing‐biao, Wu, Jia‐shun, Yang, Xiao, Tang, Ya‐jie, Chen, Yu, Tang, Ya‐ling, Liang, Xin‐hua, Cell Proliferation, Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma, Cell Biology, General Medicine
title Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_full Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_fullStr Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_full_unstemmed Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_short Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_sort hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor a mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
title_unstemmed Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
topic Cell Biology, General Medicine
url http://dx.doi.org/10.1111/cpr.12600