Astragaloside IV inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition of oral cancer cells by aggravating autophagy
Oral cancer is one usual tumor that sorely affects the health of people and even result into death. Astragaloside IV (AS-IV) is one of the major components of Astragalus membranaceus extract, and has been identified to exhibit ameliorative functions in some cancers. Nevertheless, the regulatory impa...
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Veröffentlicht in: | Tissue & cell 2024-10, Vol.90, p.102524, Article 102524 |
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Sprache: | eng |
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Zusammenfassung: | Oral cancer is one usual tumor that sorely affects the health of people and even result into death. Astragaloside IV (AS-IV) is one of the major components of Astragalus membranaceus extract, and has been identified to exhibit ameliorative functions in some cancers. Nevertheless, the regulatory impacts and correlative pathways of AS-IV in oral cancer remain vague. In this study, it was discovered that cell growth was gradually weakened with the increased dose of AS-IV (25, 50 and 100 μM). Additionally, it was uncovered that AS-IV restrained the EMT progress in oral cancer. The cell migration and invasion abilities were both gradually alleviated after AS-IV treatment in a dose-dependent manner. Moreover, AS-IV accelerated autophagy through intensifying LC3II/LC3I level and LC3B fluorescence intensity. At last, it was clarified that AS-IV triggered the AMPK pathway and retarded the AKT/mTOR pathway. In conclusion, AS-IV restrained cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress in oral cancer by aggravating autophagy through modulating the AMPK and AKT/mTOR pathways. This work may offer novel evidence on AS-IV in the treatment of oral cancer.
•AS-IV weakened cell growth in oral cancer.•AS-IV restrained the EMT progress in oral cancer.•AS-IV attenuated the migration and invasion abilities in oral cancer.•AS-IV accelerated autophagy in oral cancer.•AS-IV triggered the AMPK pathway and retarded the AKT/mTOR pathway. |
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ISSN: | 0040-8166 1532-3072 1532-3072 |
DOI: | 10.1016/j.tice.2024.102524 |