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Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial‐mesenchymal transition in salivary adenoid cystic carcinoma
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Zeitschriftentitel: | Cell Proliferation |
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Personen und Körperschaften: | , , , , , , , , , , , , , , , , |
In: | Cell Proliferation, 52, 2019, 3 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
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 |
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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 |
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Biologie |
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Wiley, 2019 |
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2019 |
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Cell Proliferation |
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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> |
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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 |
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container_title | Cell Proliferation |
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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> |
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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 |
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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 |