ArticleOpen medicine (Warsaw, Poland)2023
AS-IV enhances the antitumor effects of propofol in NSCLC cells by inhibiting autophagy.
Article in Open medicine (Warsaw, Poland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Propofol regulates METTL3-mediated PARP-1 mScientific reports · 2026Article
- Astragaloside IV Co-Loaded Osimertinib Liposomes Alleviate EGFR-TKI Resistance in Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Article
- Mechanism of astragaloside A against lung adenocarcinoma based on network pharmacology combined with molecular dynamics simulation technique.Scientific reports · 2025Article
- Astragaloside IV inhibits nasopharyngeal carcinoma progression by suppressing the SATB2/Wnt signaling axis.Toxicology research · 2025Article
- Astragaloside IV augments anti-PD-1 therapy to suppress tumor growth in lung cancer by remodeling the tumor microenvironment.European journal of histochemistry : EJH · 2024Article
- Integrative approach using network pharmacology, bioinformatics, and experimental methods to explore the mechanism of cantharidin in treating colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Regulatory role of the miR-142-3p/Translational lung cancer research · 2024Article
- The potential anti-tumor effect of anesthetics on cancer by regulating autophagy.Frontiers in pharmacology · 2024Review
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Authors and funding
6 authors.
Funding
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Abstract
Non-small cell lung cancer (NSCLC) is one of the most lethal malignant tumors. It has been shown that the general anesthetic agents, propofol and astragaloside IV (AS-IV) both exert antitumor effects in NSCLC. However, the effects of the combination of propofol with AS-IV in NSCLC remain unclear. Cell counting kit-8, and EdU and Transwell assays were performed to evaluate NSCLC cell viability, proliferation, and migration. Cell apoptosis and autophagy were observed by flow cytometric analysis and TUNEL and LC3 staining, respectively. AS-IV notably enhanced the anti-proliferative, pro-apoptotic, and anti-migratory properties of propofol in NSCLC cells. Moreover, AS-IV remarkably facilitated the anti-autophagy effect of propofol in NSCLC cells by downregulating LC3, Beclin 1, and ATG5. Significantly, the pro-apoptotic ability of the AS-IV/propofol combination in NSCLC cells was further enhanced by the autophagy inhibitor 3-MA, suggesting that autophagy plays a tumor-promoting role in NSCLC cells. Collectively, AS-IV could facilitate the antitumor abilities of propofol in NSCLC cells by inhibiting autophagy. These findings may be beneficial for future studies on the use of AS-IV and propofol for the treatment of NSCLC.
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