ArticleClinical and experimental pharmacology & physiology2022
Propofol suppresses cell proliferation in gastric cancer cells through NRF2-mediated polyol pathway.
Article in Clinical and experimental pharmacology & physiology, 2022. 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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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
6 citing papers in PubMed, 14 citations in OpenAlex.
- The role of NRF2 in human cancers: Pre-clinical insights paving the way for clinical trials.Journal of pharmaceutical analysis · 2026Review
- Does anesthesia choice shape oncologic destiny in gastric cancer surgery?World journal of gastrointestinal oncology · 2026Article
- Dexmedetomidine induces immunogenic cancer cell death and sensitizes tumors to PD-1 blockade.Journal for immunotherapy of cancer · 2025Article
- Personalized Medicine for Classical Anesthesia Drugs and Cancer Progression.Journal of personalized medicine · 2022Review
- Propofol suppresses cell proliferation in gastric cancer cells through NRF2-mediated polyol pathway.Clinical and experimental pharmacology & physiology · 2022Article
- Effect of Propofol or Etomidate as General Anaesthesia Induction on Gastric Cancer: A Retrospective Cohort Study with 10 Years' Follow-Up.Cancer management and research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Propofol, a widely used short-acting intravenous sedative agent, has gradually gained attention due to the tumour-suppressing role and non-anaesthetic effect. Dysfunction of metabolic reprogramming has been recognised as a well-documented factor for tumour progression. The aim of this study is to explore the effect of propofol on the polyol pathway in gastric cancer cells. In this study, we found that propofol treatment led to a significant downregulation of cell proliferation in BGC823 and GES-1 cells, which was attributed to the decreased AR-mediated polyol pathway. Both aldo-keto reductase family 1, member B1 (AKR1B1) and AKR1B10 were significantly reduced in BGC823 and GES-1 cells in response to propofol stimulation, leading to decreased AR activity and sorbitol level. Addition of sorbitol could reverse the inhibitory effect of propofol on cell proliferation. Mechanically, propofol treatment drastically inhibited phosphorylation and nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 (NRF2), subsequently decreased the binding of NRF2 to AR promoter. Overexpression of NRF2 resulted in the recovery of AR expression in gastric cancer cell with propofol treatment. Taken together, these finding showed that propofol suppressed cell proliferation in BGC823 and GES-1 cell through NRF2-mediated polyol pathway, which would aid the selection of sedation for patients with gastric cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.