ADAR1 silencing-induced HUVEC apoptosis is mediated by FGFR2 under hypoxia stress
Authors Jiang Y, Wang Z, Chen X, Wang W, Wang X
Received 24 July 2018
Accepted for publication 1 October 2018
Published 10 December 2018 Volume 2018:12 Pages 4181—4189
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 4
Editor who approved publication: Professor Jianbo Sun
Yun Jiang,1 Zhancheng Wang,1 Xu Chen,1 Wei Wang,1 Xiaowei Wang2
1Department of Cardiology, The Eighth People’s Hospital of Shanghai, Shanghai 200233, China; 2Shanghai Weiang Info Tech Ltd., Shanghai 200233, China
Background: The adenosine deaminase acting on RNA 1 (ADAR1) specifically deaminates adenosine to inosine in double-stranded RNA (dsRNA). Emerging evidence indicated that under hypoxia condition, such as tumor microenvironment, ADAR1 level was increased. Interestingly, we found FGFR2 was also increased under hypoxia stress. The purpose of this study was to investigate the regulation mechanism of ADAR1 and the potential role of ADAR1–FGFR2 axis in cell proliferation and apoptosis.
Methods: Using human umbilical vein endothelial cells as cellular model, we explored the function of ADAR1 in regulating cell survival.
Results: We found manipulation of FGFR2 activity could override the cellular effect of ADAR1, suggesting FGFR2 could be a potential effector of ADAR1. Moreover, our results revealed that PI3K-Akt pathway was involved in ADAR1–FGFR2 axis-induced cell proliferation.
Conclusion: In summary, this study supported the notion that ADAR1 could play a role in tumor cell proliferation, which was mediated by FGFR2.
Keywords: ADAR1, HUVEC, FGFR2, apoptosis, hypoxia, PI3K-Akt pathway
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