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Inhibitory effect of ginsenglactone A from Panax ginseng on the tube formation of human umbilical vein endothelial cells and migration of human ovarian cancer cells

  • Dahae, Lee (College of Korean Medicine, Gachon University) ;
  • Ranhee, Kim (Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University) ;
  • So-Ri, Son (Department of Biomedical and Pharmaceutical Sciences, Graduate School, Kyung Hee University) ;
  • Ji-Young, Kim (Department of Biomedical and Pharmaceutical Sciences, Graduate School, Kyung Hee University) ;
  • Sungyoul, Choi (College of Korean Medicine, Gachon University) ;
  • Ki Sung, Kang (College of Korean Medicine, Gachon University) ;
  • Dae Sik, Jang (Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University)
  • Received : 2022.05.03
  • Accepted : 2022.08.09
  • Published : 2023.03.02

Abstract

Background: Here, we aimed to assess the inhibitory effect of a new compound from Panax ginseng on the migration of human ovarian cancer cells and tube formation of human umbilical vein endothelial cells (HUVECs). Methods: A new compound, ginsenglactone A (1), was isolated from ginseng roots, together with seven known compounds (2-8). Spectroscopic data were used to elucidate the chemical structure of 1. The tubular structure formation in HUVECs was assessed by Mayer's hematoxylin staining. The migration of A2780 cells was evaluated using the scratch wound healing assay. Results: HUVECs treated with 1 had the statistically significant decrease in tubular structure formation compared to the HUVECs treated with compounds 2-8. This effect was enhanced by co-treatment with inhibitors for phosphatidylinositol 3-kinase (PI3K) (LY294002) and extracellular signal-regulated kinase (ERK) (U0126). Treatment with 1 decreased the expression of phosphorylation of ERK, PI3K, vascular endothelial growth factor receptor2 (VEGFR2), Akt, and mammalian target of rapamycin (mTOR). In addition, the ability of A2780 cells to cover the scratched area were also decreased. This effect was enhanced by co-treatment with U0126. Lastly, treatment with 1 decreased the phosphorylation of ERK, matrix metalloproteinase-9 (MMP-9), and MMP-2. Conclusion: These results suggest that ginsenglactone A is a potential inhibitor of HUVEC tubular structure formation and A2780 cellular migration, which may be helpful for understanding its anticancer mechanism.

Keywords

Acknowledgement

This work was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT (MSIT), Republic of Korea (grant number: NRF-2019R1A2C1083945). This study was also funded by KIST BlueBell Project (2E31920).

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