ArticleJournal of dental sciences2025
miR-376a/Neuropilin-1 axis mediates the cancer stemness in oral squamous cell carcinoma-an in vitro study.
Article in Journal of dental sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- From Environmental Risk to Cancer Stemness: Epigenetic Regulation in Oral Squamous Cell Carcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: The incidence of oral cancer has been steadily increased over the years. Recent researches indicated that exploring oral cancer stem cells (CSCs) characterized by self-renewal, pluripotency, and aggressiveness have emerged as a promising strategy for predicting oral squamous cell carcinoma (OSCC) recurrence and metastasis. Previous studies have demonstrated that microRNAs regulate cancer stemness. However, the mechanisms that miR-376a/neuropilin-1 (NRP1) axis influences CSC traits have not yet been fully understood. Therefore, an in-depth investigation was conducted in this study. Materials and methods: miR-376a expression in CSCs derived from OSCC cell line SAS was quantified by quantitative real-time polymerase chain reaction. Aldehyde dehydrogenase 1 (ALDH1) activity and CD44 expression were assessed via flow cytometry. The CSC phenotype was characterized through self-renewal, migration, and colony formation assays. A luciferase reporter assay was used to confirm the direct interaction between miR-376a and NRP1. Results: We found that miR-376a expression was downregulated in SAS-CSCs. Overexpression of miR-376a significantly reduced several CSC phenotypes including ALDH1 activity, CD44 expression, migration, and colony-forming abilities, respectively ( Conclusion: Within the limitations of our findings, miR-376a/NRP1 axis may play a crucial role in stemness of OSCC. Targeting this pathway could represent a promising strategy to inhibit OSCC progression.
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