PUBLICATION
MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells
- Authors
- Wu, X.D., Guo, T., Liu, L., Wang, C., Zhang, K., Liu, H.Q., Wang, F., Bai, W.D., Zhang, M.Y.
- ID
- ZDB-PUB-170924-11
- Date
- 2017
- Source
- Oncotarget 8: 58072-58085 (Journal)
- Registered Authors
- Wang, Chao
- Keywords
- angiogenesis, ginsenoside Rg1, miR-23a, runt-related transcription factor 2, vascular endothelial growth factor
- MeSH Terms
- none
- PubMed
- 28938538 Full text @ Oncotarget
Citation
Wu, X.D., Guo, T., Liu, L., Wang, C., Zhang, K., Liu, H.Q., Wang, F., Bai, W.D., Zhang, M.Y. (2017) MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells. Oncotarget. 8:58072-58085.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping