Stereospecific effects of ginsenoside 20-Rg3 inhibits TGF-beta 1-induced epithelial-mesenchymal transition and suppresses lung cancer migration, invasion and anoikis resistance
- Authors
- Kim, Young-Joo; Choi, Won-Il; Jeon, Bu-Nam; Choi, Kyung-Chul; Kim, Kunhong; Kim, Tae-Jin; Ham, Jungyeob; Jang, Hyuk Jai; Kang, Ki Sung; Ko, Hyeonseok
- Issue Date
- 1-Aug-2014
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Ginsenoside 20(R)-Rg3; Epithelial-mesenchymal transition (EMT); Transforming growth factor-beta 1 (TGF-beta 1); Lung cancer; Metastasis
- Citation
- TOXICOLOGY, v.322, pp.23 - 33
- Journal Title
- TOXICOLOGY
- Volume
- 322
- Start Page
- 23
- End Page
- 33
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12387
- DOI
- 10.1016/j.tox.2014.04.002
- ISSN
- 0300-483X
- Abstract
- The epithelial mesenchymal transition (EMT) is a pivotal cellular process during which epithelial polarized cells become motile mesenchymal-appearing cells, which, in turn, promotes the metastatic potential of cancer. Ginseng is a perennial plant belonging to the genus Panax that exhibits a wide range of pharmacological and physiological activities. Ginsenosides 20-Rg3, which is the active component of ginseng, has various medical effects, such as anti-tumorigenic, anti-angiogenesis, and anti-fatiguing activities. In addition, ginsenosides 20(S)-Rg3 and 20(R)-Rg3 are epimers, and this epimerization is produced by steaming. However, the possible role of 20(S)-Rg3 and 20(R)-Rg3 in the EMT is unclear. We investigated the effect of 20(S)-Rg3 and 20(R)-Rg3 on the EMT. Transforming growth factor-beta 1 (TGF-beta 1) induces the EMT to promote lung adenocarcinoma migration, invasion, and anoikis resistance. To understand the repressive role of 20(S)-Rg3 and 20(R)-Rg3 in lung cancer migration, invasion, and anoikis resistance, we investigated the potential use of 20(S)-Rg3 and 20(R)-Rg3 as inhibitors of TGF-beta 1-induced EMT development in A549 lung cancer cells in vitro. Here, we show that 20(R)-Rg3, but not 20(S)-Rg3, markedly increased expression of the epithelial marker E-cadherin and repressed Snail upregulation and expression of the mesenchymal marker vimentin during initiation of the TGF-beta 1-induced EMT. 20(R)-Rg3 also inhibited the TGF-beta 1-induced increase in cell migration, invasion, and anoikis resistance of A549 lung cancer cells. Additionally, 20(R)-Rg3 markedly inhibited TGF-beta 1-regulated matrix metalloproteinase-2 and activation of Smad2 and p38 mitogen activated protein kinase. Taken together, our findings provide new evidence that 20(R)-Rg3 suppresses lung cancer migration, invasion, and anoikis resistance in vitro by inhibiting the TGF-beta 1-induced EMT. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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