ArticleOncology letters2022
Propofol inhibits the malignant development of osteosarcoma U2OS cells via AMPK/FΟΧO1-mediated autophagy.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Comparison of total intravenous anesthesia and combined inhalation and intravenous anesthesia on survival after tumor surgery: a propensity score matched cohort study.Frontiers in medicine · 2026Article
- The potential anti-tumor effect of anesthetics on cancer by regulating autophagy.Frontiers in pharmacology · 2024Review
- CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has previously been reported that propofol regulates the development of human osteosarcoma (OS). However, the specific molecular mechanisms underlying the effect of propofol on OS remain poorly understood. Therefore, the aim of the present study was to explore the effects of propofol on OS U2OS cells and the potential underlying mechanism. The Cell Counting Kit-8 and colony formation assays were performed to assess cell viability and proliferation. Furthermore, cell apoptosis was assessed using the TUNEL assay and western blotting. Wound healing and Transwell assays were performed to evaluate OS cell migration and invasion abilities, respectively. The protein expression levels of epithelial-mesenchymal transition (EMT)-, autophagy- and adenosine monophosphate-activated protein kinase (AMPK)/FOXO1 signaling pathway-related proteins were also determined using western blotting. The results demonstrated that propofol significantly reduced the viability of OS cells and promoted autophagy in a dose-dependent manner. Moreover, cell treatment with propofol significantly enhanced the protein expression levels of phosphorylated (p)-AMPK and FOXO1, while decreasing the protein levels of p-FOXO1. Furthermore, treatment with propofol significantly suppressed cell viability, migration and invasion abilities and the EMT of OS cells, and potentially promoted cell apoptosis via inducing autophagy via the AMPK/FOXO1 signaling pathway. In summary, the present study indicated that propofol potentially had an inhibitory effect on the development of OS cells via AMPK/FOXO1-mediated autophagy. These results have therefore provided an experimental basis for further studies into the therapeutic effect of propofol on OS.
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