ArticleThe Journal of international medical research2021
Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3.
Article in The Journal of international medical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Does anesthesia choice shape oncologic destiny in gastric cancer surgery?World journal of gastrointestinal oncology · 2026Article
- FKH domain-mediated nuclear FOXP3 suppresses gastric cancer malignancy via c-MYC/CDKN1A regulation, EMT inhibition, and PI3K/AKT signaling modulation.Molecular and cellular biochemistry · 2026Article
- Sevoflurane induces CaCytotechnology · 2025Article
- Effects of perioperative anesthetics on the postoperative prognosis of patients undergoing surgery for cervical cancer.Frontiers in pharmacology · 2025Review
- Article
- Sevoflurane inhibits cholangiocarcinoma via Wnt/β-catenin signaling pathway.BMC gastroenterology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePrevious studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells.
methodsGC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively.
resultsFOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells.
conclusionsSevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion
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