ArticleMolecular biotechnology2025
Sufentanil Suppresses Cell Carcinogenesis Via Targeting miR-186-5p/HMGB1 Axis and Wnt/β-Catenin Pathway in Non-Small-Cell Lung Cancer.
Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Overexpression of miR-320-3p, miR-381-3p, and miR-27a-3p Suppresses Genes Related to Midline Facial Cleft in Mouse Cranial Neural Crest Cells.International journal of molecular sciences · 2025Article
- HMGB1 as a Key Mediator in Malignant Mesothelioma and a Potential Target for Asbestos-Related Cancer Therapy.Toxics · 2025Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sufentanil is a common opioid anesthetic agent, which exerts anti-cancer properties in several cancer types. However, its action mechanisms in non-small cell lung cancer (NSCLC) are unclear. Therefore, the present study investigated the pharmacological effect of sufentanil on miRNAs in NSCLC treatment. In this study, after treatment with sufentanil, the proliferation, migration, invasion and apoptosis of A549 and H1299 NSCLC cell lines were measured by cell counting kit-8 (CCK-8) assay, colony formation assay, transwell assays and flow cytometry. Quantitative real time polymerase chain reaction (qRT-PCR) was utilized to detect the expression of miR-186-5p and high mobility group box-1 (HMGB1), and their interaction was analyzed using luciferase reporter assay. The proteins of HMGB1, and apoptosis- and Wnt/β-catenin pathway-related factors were detected by western blot. It was demonstrated that sufentanil significantly upregulated miR‑186‑5p to restrict NSCLC cell proliferation, migration, invasion, and boost apoptosis in vitro. Mechanically, miR-186-5p interacted with HMGB1 and negatively regulated HMGB1 in NSCLC cells. Furthermore, rescue assay showed that sufentanil exerted antitumor activities by upregulating miR-186-5p, which targeted HMGB1 and restrained Wnt/β-catenin signal pathway in NSCLC cells. In conclusion, these results suggested that sufentanil disrupts the oncogenicity of NSCLC cells by regulating miR-186-5p/HMGB1/β-catenin axis, providing a promising implication for the anti-oncogenic effect of sufentanil.
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Registered trials
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