ArticleHistology and histopathology2024
Upregulation of LY6K induced by FTO-mediated demethylation promotes the tumorigenesis and metastasis of oral squamous cell carcinoma via CAV-1-mediated ERK1/2 signaling activation.
Article in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Schistosoma haematobium infection is associated with oncogenic gene expression in Cervical Mucosa, with enhanced effects following treatment: A pilot study.PLoS neglected tropical diseases · 2025Article
- Multi-omics exploration of CAV1Discover oncology · 2025Article
- The mechanistic study of codonopsis pilosula on laryngeal squamous cell carcinoma based on network pharmacology and experimental validation.Frontiers in pharmacology · 2025Article
- Silencing LY6K Suppresses CD44Current issues in molecular biology · 2024Article
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3 authors at 1 institution in 1 country.
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Abstract
Lymphocyte antigen 6 complex locus K (LY6K) has been demonstrated to play a significant role in cancers and identified as a therapeutic biomarker for head and neck squamous cell carcinoma. However, the role of LY6K in oral squamous cell carcinoma (OSCC) has not been explored. The current study discovered that LY6K was aberrantly upregulated in OSCC cell lines and tissues and that high LY6K expression significantly correlated with poorer survival of OSCC patients. Through stable knockdown of LY6K, we found that the growth, colony formation, migration, and invasion of OSCC cells were substantially suppressed. In addition, tumor growth and lung metastasis
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