MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells
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Xiao-Dong Wu1,*, Ting Guo4,*, Li Liu5,*, Chao Wang5, Kun Zhang1,6, Han-Qiang Liu4, Feng Wang4, Wen-Dong Bai7 and Meng-Yao Zhang1,2,3
1Department of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi’an 710032, China
2Beijing Institute of Biotechnology, Beijing 100071, China
3Department of Clinical Immunology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
4Department of Nutrition and Food Hygiene, Fourth Military Medical University, Xi’an 710032, China
5Department of Stomatology, PLA General Hospital, Beijing 100700, China
6College of Life Science and Bioengineering, School of Science, Beijing Jiaotong University, Beijing 100044, China
7Clinical Laboratory Medicine Center, Xinjiang Command General Hospital of PLA, Urumqi 830000, China
*These authors have contributed equally to this work
Meng-Yao Zhang, email: email@example.com
Wen-Dong Bai, email: firstname.lastname@example.org
Feng Wang, email: email@example.com
Keywords: angiogenesis, ginsenoside Rg1, miR-23a, runt-related transcription factor 2, vascular endothelial growth factor
Received: May 01, 2017 Accepted: June 19, 2017 Published: July 22, 2017
Rg1 is a predominant protopanaxatriol-type of ginsenoside found in Panax ginseng, and it has been shown to have anti-cancer effects in multiple types of cancer cells. However, Rg1 also induces the expression of proangiogenic factors, such as vascular endothelial growth factor (VEGF-A), in endothelial cells. Unfortunately, angiogenesis positively correlates with cancer development. In this study, we identified RUNX2 as a regulator of ginsenoside Rg1-induced angiogenesis for the first time. We found that RUNX2 was directly targeted and regulated by miR-23a. Additionally, miR-23a was shown to inhibit angiogenesis in both human umbilical vein endothelial cells (HUVECs) and in zebrafish. Furthermore, a decrease in RUNX2 expression resulted in translational repression of VEGF-A in HUVECs. Taken together, this study identified a MiR-23a/RUNX2/VEGF-A pathway in angiogenesis and shed light on the molecular mechanism of Rg1-induced angiogenesis. Thus, RUNX2 might be a potential therapeutic target in Rg1-mediated angiogenesis in cancer.
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