Journal
FRONTIERS IN ONCOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2020.609275
Keywords
lung cancer cells; toxicarioside O; cell proliferation; epithelial-mesenchymal transition; trophoblast cell surface antigen 2
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Funding
- Natural Science Foundation of Hainan Province [819MS062]
- National Natural Science Foundation of China [81860429, 81660004, 81760634, 81860650, 81673346]
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The study found that TCO effectively inhibits proliferation and induces apoptosis in lung cancer cells, while also suppressing cell migration and the EMT program. Mechanistically, TCO inhibits the PI3K/Akt pathway and EMT program by reducing Trop2 expression, indicating its potential as an anticancer agent.
Toxicarioside O (TCO), a natural product derived from Antiaris toxicaria, has been identified to be a promising anticancer agent. In this study, we aimed to investigate the effect of TCO on the proliferation and epithelial-mesenchymal transition (EMT) of lung cancer cells and its molecular mechanisms. Here, we indicated that TCO inhibits the proliferation of lung cancer cells both in vitro and in vivo. Our results demonstrated that TCO induces apoptosis in lung cancer cells. Moreover, we found that TCO suppresses EMT program and inhibits cell migration in vitro. Mechanistically, TCO decreases the expression of trophoblast cell surface antigen 2 (Trop2), resulting in inhibition of the PI3K/Akt pathway and EMT program. Overexpression of Trop2 rescues TCO-induced inhibition of cell proliferation and EMT. Our findings demonstrate that TCO markedly inhibits cell proliferation and EMT in lung cancer cells and provides guidance for its drug development.
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