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HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma

BACKGROUND: High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a numbe...

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Autores principales: Wu, Cun-Zao, Zheng, Jian-Jian, Bai, Yong-Heng, Xia, Peng, Zhang, Hai-Cong, Guo, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078191/
https://www.ncbi.nlm.nih.gov/pubmed/30122942
http://dx.doi.org/10.2147/OTT.S167197
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author Wu, Cun-Zao
Zheng, Jian-Jian
Bai, Yong-Heng
Xia, Peng
Zhang, Hai-Cong
Guo, Yong
author_facet Wu, Cun-Zao
Zheng, Jian-Jian
Bai, Yong-Heng
Xia, Peng
Zhang, Hai-Cong
Guo, Yong
author_sort Wu, Cun-Zao
collection PubMed
description BACKGROUND: High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers. METHODS: CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively. RESULTS: In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth. CONCLUSION: Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC.
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spelling pubmed-60781912018-08-17 HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma Wu, Cun-Zao Zheng, Jian-Jian Bai, Yong-Heng Xia, Peng Zhang, Hai-Cong Guo, Yong Onco Targets Ther Original Research BACKGROUND: High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers. METHODS: CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively. RESULTS: In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth. CONCLUSION: Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC. Dove Medical Press 2018-08-01 /pmc/articles/PMC6078191/ /pubmed/30122942 http://dx.doi.org/10.2147/OTT.S167197 Text en © 2018 Wu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Wu, Cun-Zao
Zheng, Jian-Jian
Bai, Yong-Heng
Xia, Peng
Zhang, Hai-Cong
Guo, Yong
HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title_full HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title_fullStr HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title_full_unstemmed HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title_short HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
title_sort hmgb1/rage axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078191/
https://www.ncbi.nlm.nih.gov/pubmed/30122942
http://dx.doi.org/10.2147/OTT.S167197
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