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VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

Background: Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed...

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Autores principales: Chen, Li, Lin, Guoxiang, Chen, Kaihua, Liang, Renba, Wan, Fangzhu, Zhang, Chuxiao, Tian, Ge, Zhu, Xiaodong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646165/
https://www.ncbi.nlm.nih.gov/pubmed/33193893
http://dx.doi.org/10.7150/jca.46429
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author Chen, Li
Lin, Guoxiang
Chen, Kaihua
Liang, Renba
Wan, Fangzhu
Zhang, Chuxiao
Tian, Ge
Zhu, Xiaodong
author_facet Chen, Li
Lin, Guoxiang
Chen, Kaihua
Liang, Renba
Wan, Fangzhu
Zhang, Chuxiao
Tian, Ge
Zhu, Xiaodong
author_sort Chen, Li
collection PubMed
description Background: Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed to examine the biological function of VEGF in NPC metastasis and its underlying mechanism. Methods: We used western blotting and qPCR to examine the difference in VEGF expression between NPC cells and the immortalized nasopharyngeal epithelial cell line NP69. Wound healing assays, transwell assays and animal experiments were used to further verify the role of VEGF in the invasion and migration of NPC cells. The protein levels of the epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) family were analysed by immunofluorescence (IF) and western blotting. Enzyme-linked immunosorbent assay (ELISA) and transwell assays were used to determine whether VEGF enhanced the invasion and migration of NPC cells in an autocrine manner. Western blotting was used to examine how autocrine VEGF-VEGFR2 signalling regulated EMT and MMPs. Results: We observed higher levels of VEGF in NPC cells than that in NP69 cells and identified an association between high VEGF levels and tumour invasion and migration. Mechanistically, the VEGF-mediated increase in EMT markers, MMP2 and MMP9 promoted NPC cell invasion and migration. Additionally, NPC cells secreted VEGF to promote cell invasion, migration and angiogenesis. Autocrine VEGF-VEGFR2 signalling increased ERK1/2 phosphorylation, promoted EMT process and MMPs at the indicated times. Conclusion: This study revealed that VEGF plays a role in controlling NPC cell metastasis by regulating EMT markers and MMPs in an autocrine manner.
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spelling pubmed-76461652020-11-12 VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma Chen, Li Lin, Guoxiang Chen, Kaihua Liang, Renba Wan, Fangzhu Zhang, Chuxiao Tian, Ge Zhu, Xiaodong J Cancer Research Paper Background: Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed to examine the biological function of VEGF in NPC metastasis and its underlying mechanism. Methods: We used western blotting and qPCR to examine the difference in VEGF expression between NPC cells and the immortalized nasopharyngeal epithelial cell line NP69. Wound healing assays, transwell assays and animal experiments were used to further verify the role of VEGF in the invasion and migration of NPC cells. The protein levels of the epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) family were analysed by immunofluorescence (IF) and western blotting. Enzyme-linked immunosorbent assay (ELISA) and transwell assays were used to determine whether VEGF enhanced the invasion and migration of NPC cells in an autocrine manner. Western blotting was used to examine how autocrine VEGF-VEGFR2 signalling regulated EMT and MMPs. Results: We observed higher levels of VEGF in NPC cells than that in NP69 cells and identified an association between high VEGF levels and tumour invasion and migration. Mechanistically, the VEGF-mediated increase in EMT markers, MMP2 and MMP9 promoted NPC cell invasion and migration. Additionally, NPC cells secreted VEGF to promote cell invasion, migration and angiogenesis. Autocrine VEGF-VEGFR2 signalling increased ERK1/2 phosphorylation, promoted EMT process and MMPs at the indicated times. Conclusion: This study revealed that VEGF plays a role in controlling NPC cell metastasis by regulating EMT markers and MMPs in an autocrine manner. Ivyspring International Publisher 2020-10-21 /pmc/articles/PMC7646165/ /pubmed/33193893 http://dx.doi.org/10.7150/jca.46429 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Chen, Li
Lin, Guoxiang
Chen, Kaihua
Liang, Renba
Wan, Fangzhu
Zhang, Chuxiao
Tian, Ge
Zhu, Xiaodong
VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title_full VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title_fullStr VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title_full_unstemmed VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title_short VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma
title_sort vegf promotes migration and invasion by regulating emt and mmps in nasopharyngeal carcinoma
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646165/
https://www.ncbi.nlm.nih.gov/pubmed/33193893
http://dx.doi.org/10.7150/jca.46429
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