Asiaticoside Inhibits Growth and Metastasis in Non-Small Cell Lung Cancer by Disrupting EMT via Wnt/β-Catenin Pathway.

Autor: Zhang Y; Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, China., Liu J; Department of Radiography, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China., Yang G; Department of Cardiothoracic Surgery, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China., Zou J; Department of Radiography, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China., Tan Y; Department of Cardiothoracic Surgery, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China., Xi E; Department of Cardiothoracic Surgery, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China., Geng Q; Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, China., Wang Z; Department of Cardiothoracic Surgery, Central Theater Command General Hospital of Chinese People's Liberation Army, Wuhan, China.
Jazyk: angličtina
Zdroj: Environmental toxicology [Environ Toxicol] 2024 Nov; Vol. 39 (11), pp. 4859-4870. Date of Electronic Publication: 2024 Jun 18.
DOI: 10.1002/tox.24359
Abstrakt: Non-small cell lung cancer (NSCLC) is the primary inducer of cancer-related death worldwide. Asiaticoside (ATS) is a triterpenoid saponin that has been indicated to possess an antitumor activity in several malignancies. Nonetheless, its detailed functions in NSCLC remain unclarified. In this study, NSCLC cells were exposed to various doses of ATS. Functional experiments were employed to estimate the ATS effect on NSCLC cell behaviors. Western blotting was implemented for protein expression evaluation. A xenograft mouse model was established to assess the ATS effect on NSCLC in vivo. The results showed that ATS restrained NSCLC cell proliferation, cell cycle progression, migration, and invasiveness. ATS reversed TGF-β-induced promotion in epithelial-mesenchymal transition (EMT). Mechanistically, ATS inhibited Wnt/β-catenin signaling in NSCLC. Upregulating β-catenin restored ATS-mediated suppression of NSCLC cell aggressiveness. Moreover, ATS administration repressed tumorigenesis in tumor-bearing mice. In conclusion, ATS represses growth and metastasis in NSCLC by blocking EMT via the inhibition of Wnt/β-catenin signaling.
(© 2024 Wiley Periodicals LLC.)
Databáze: MEDLINE
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