Back to Journals » OncoTargets and Therapy » Volume 11

SOX5 induces lung adenocarcinoma angiogenesis by inducing the expression of VEGF through STAT3 signaling

Authors Chen X, Zheng Q, Li W, Lu Y, Ni Y, Ma L, Fu Y

Received 7 June 2018

Accepted for publication 24 July 2018

Published 11 September 2018 Volume 2018:11 Pages 5733—5741

DOI https://doi.org/10.2147/OTT.S176533

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Leo Jen-Liang Su


Xin Chen,1,* Qi Zheng,1,* Weidong Li,1 Yuan Lu,1 Yiming Ni,1 Liang Ma,1 Yufei Fu2

1Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang 310003, P. R. China; 2Zhejiang Key Laboratory of Gastro-Intestinal Pathophysiology, Zhejiang Hospital of Traditional Chinese Medicine, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P. R. China

*These authors contributed equally to this work

Background and objectives: Angiogenesis is the main cause of lung adenocarcinoma (LAC) poor prognosis. This study aimed to investigate the effect of sex-determining region Y-box protein 5 (SOX5) expression on angiogenesis of LAC and explore its possible mechanism.
Patients and methods: The effect on angiogenesis was tested by tube formation assays using human umbilical vein endothelial cells cocultured with A549 cells. Lentivirus shRNA of SOX5 and lentivirus of SOX5 overexpression system were used to establish LAC cell lines, which expressed SOX5 of different levels. SOX5 downstream signaling targets were analyzed by real-time qPCR and Western blot. We collected 90 LAC cases and the tissues were examined by immunohistochemistry for SOX5 and vascular endothelial growth factor (VEGF).
Results: We found that SOX5 overexpression in A549 cells significantly promoted tube formation capacity of the cocultured human umbilical vein endothelial cells. SOX5 increased VEGF expression and signal transducer activator of transcription 3 phosphorylation; however, SOX5 had no effect on extracellular signal-regulated kinase and protein kinase B pathway. Furthermore, the expression of SOX5 and VEGF had a significantly positive correlation (r=0.399, P=0.001) according to the tissue microarray data.
Conclusion: These findings suggest that SOX5 induces angiogenesis by activating signal transducer activator of transcription 3/VEGF signaling and confer its candidacy as a potential therapeutic target in LAC.

Keywords: SOX5, VEGF, STAT3, angiogenesis, lung adenocarcinoma, tissue microarray, tube formation

Creative Commons License 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. 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]