Abstract
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.
Highlights
Toxicarioside O (TCO) is one of the cardenolides isolated from the seeds of Antiaris toxicaria [1]
Our findings indicated that TCO inhibits cell proliferation in lung cancer cells
O (TCO) is one of the cardenolides isolated from the seeds of Antiaris toxicaria that exhibits potential anticancer activities
Summary
Toxicarioside O (TCO) is one of the cardenolides isolated from the seeds of Antiaris toxicaria [1]. Accumulating evidence has indicated that cardenolides have significant anticancer effects in various types of human cancer cell [4, 5]. Consistent with these findings, TCO exhibits significant cytotoxicity against hepatocellular carcinoma cell line SMMC-7721 and human. We have previously demonstrated that TCO inhibits cell proliferation and induces protective autophagy in colorectal cancer cells [6]. The effect of TCO on the proliferation and epithelial-mesenchymal transition (EMT) of lung cancer cells and its molecular mechanisms remain largely unknown
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