Ginsenosides Rk1 and Rg5 inhibit transforming growth factor-β1-induced epithelial-mesenchymal transition and suppress migration, invasion, anoikis resistance, and development of stem-like features in lung cancer
| Autor: | Seon-Jun Choi, Pilju Choi, Taejung Kim, Hyeonseok Ko, Young-Seok Kim, Won-Chul Lim, Cheol Hee Yoon, Bong Geun Song, Jungyeob Ham, Hyunhee Kim, Young-Tae Park |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Ginsenosides Transforming growth factor β1 Stem cell marker Biochemistry Genetics and Molecular Biology (miscellaneous) 03 medical and health sciences 0302 clinical medicine lcsh:Botany medicine Anoikis Epithelial–mesenchymal transition A549 cell biology Chemistry CD44 Cancer Transforming growth factor beta medicine.disease Epithelial-mesenchymal transition Panax ginseng Meyer lcsh:QK1-989 030104 developmental biology Complementary and alternative medicine 030220 oncology & carcinogenesis biology.protein Cancer research Lung cancer Biotechnology Transforming growth factor Research Article |
| Zdroj: | Journal of Ginseng Research, Vol 45, Iss 1, Pp 134-148 (2021) Journal of Ginseng Research |
| ISSN: | 1226-8453 |
| Popis: | Background Lung cancer has a high incidence worldwide, and most lung cancer-associated deaths are attributable to cancer metastasis. Although several medicinal properties of Panax ginseng Meyer have been reported, the effect of ginsenosides Rk1 and Rg5 on epithelial-mesenchymal transition (EMT) stimulated by transforming growth factor beta 1 (TGF- β1) and self-renewal in A549 cells is relatively unknown. Methods We treated TGF-β1 or alternatively Rk1 and Rg5 in A549 cells. We used western blot analysis, real-time polymerase chain reaction (qPCR), wound healing assay, Matrigel invasion assay, and anoikis assays to determine the effect of Rk1 and Rg5 on TGF-mediated EMT in lung cancer cell. In addition, we performed tumorsphere formation assays and real-time PCR to evaluate the stem-like properties. Results EMT is induced by TGF-β1 in A549 cells causing the development of cancer stem-like features. Expression of E-cadherin, an epithelial marker, decreased and an increase in vimentin expression was noted. Cell mobility, invasiveness, and anoikis resistance were enhanced with TGF-β1 treatment. In addition, the expression of stem cell markers, CD44, and CD133, was also increased. Treatment with Rk1 and Rg5 suppressed EMT by TGF-β1 and the development of stemness in a dose-dependent manner. Additionally, Rk1 and Rg5 markedly suppressed TGF-β1-induced metalloproteinase-2/9 (MMP2/9) activity, and activation of Smad2/3 and nuclear factor kappa B/extra-cellular signal regulated kinases (NF-kB/ERK) pathways in lung cancer cells. Conclusions Rk1 and Rg5 regulate the EMT inducing TGF-β1 by suppressing the Smad and NF-κB/ERK pathways (non-Smad pathway). |
| Databáze: | OpenAIRE |
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