ArticleJournal of dental sciences2022
miR-509 inhibits cancer stemness properties in oral carcinomas via directly targeting PlK1.
Article in Journal of dental sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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
4 citing papers in PubMed, 6 citations in OpenAlex.
- From Environmental Risk to Cancer Stemness: Epigenetic Regulation in Oral Squamous Cell Carcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Review
- miR-376a/Neuropilin-1 axis mediates the cancer stemness in oral squamous cell carcinoma-an in vitro study.Journal of dental sciences · 2025Article
- Mir-509-3p targets SLC25A13 to regulate ferroptosis and protect retinal endothelial cells in diabetic retinopathy.Acta diabetologica · 2025Article
- LncRNA SNHG5 promotes the invasion and proliferation of oropharyngeal squamous cell carcinoma by regulating the miR-21/PTEN signaling pathway.American journal of translational research · 2025Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Oral cancer is one of the common cancers worldwide. Emerging evidence has indicated that microRNAs (non-coding RNA molecules of approximately 22 nucleotides in length) are implicated in the regulation of cancer stemness. However, the functional role of microRNA-509 (miR-509) in the characteristics of oral cancer stem cells (CSCs) has not been unraveled. Materials and methods: The expression level of miR-509 in ALDH1 Results: We showed the expression of miR-509 was downregulated in the CSCs derived from oral cancer cells (SAS), and upregulation of miR-509 diminished the several CSCs features, including ALDH1 activity, self-renewal capacity, CD44 expression, migration, and colony-forming abilities. Moreover, the result from the luciferase reporter assay validated the direct binding of miR-509 to plk1. Conclusion: Our results suggest that the miR-509/plk1 axis may mediate the cancer stemness in oral cancer, and targeting this axis may attenuate the progression of oral 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.