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

Authors Wu CZ, Zheng JJ, Bai YH, Xia P, Zhang HC, Guo Y

Received 4 March 2018

Accepted for publication 26 April 2018

Published 1 August 2018 Volume 2018:11 Pages 4501—4510

DOI https://doi.org/10.2147/OTT.S167197

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 3

Editor who approved publication: Dr William Cho


Cun-Zao Wu,1 Jian-Jian Zheng,2 Yong-Heng Bai,2 Peng Xia,1 Hai-Cong Zhang,3 Yong Guo1

1Department of Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; 2Department of Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; 3Department of Pathology, The Fifth Hospital of Shijiazhuang, Shijiazhuang, China

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.

Keywords: HMGB1, RCC, apoptosis, invasion, autophagy, angiogenesis

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