ArticleScientific reports2025
H3 lysine 18 lactylation-mediated RRAS2 facilitates migration and invasion of head and neck squamous cell carcinoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Rhaponticin Blocks Glycolysis-Mediated Histone Lactylation to Suppress Tongue Squamous Cell Carcinoma via HIF-1α Activity Inhibition.The Kaohsiung journal of medical sciences · 2026Article
- Lactylation enzymes in cancer: Mechanisms and novel therapeutic approaches (Review).Oncology letters · 2026Review
- Diagnostic, Prognostic, and Predictive Molecular Biomarkers in Head and Neck Squamous Cell Carcinoma: A Comprehensive Review.Journal of clinical medicine · 2026Review
- Three-dimensional-bioprinted stiff matrix triggers PDAC radioresistance through histone H3 lysine 18 lactylation (H3K18la) potentiates RAD51 activation.Regenerative biomaterials · 2026Article
- A lactylation-related gene signature predicts metastasis and prognosis in breast cancer.Scientific reports · 2025Article
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Authors and funding
4 authors.
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Abstract
RRAS2, induced by H3 lysine 18 lactylation (H3K18la), plays a vital role in activating signal transduction pathways that control cell proliferation. However, fewer studies focused on the role of H3K18la-mediated RRAS2 in head and neck squamous cell carcinoma (HNSCC). The RRAS2 expression was obtained from various databases, and we explored the role of RRAS2 in HNSCC prognosis. We further investigated the roles of RRAS2 in the immune microenvironment and drug resistance. The roles of RRAS2 in HNSCC progression were also determined. We suggested that RRAS2 was overexpressed in various cancer types, including HNSCC. High expression of RRAS2 might play a vital role in HNSCC metastasis and prognosis. In addition, RRAS2 might mediate the infiltration of various immune cells in HNSCC. High RRAS2 expression was positively related to chemotherapy resistance and tumor mutation burden (TMB), a biomarker for poor immunotherapy response. Furthermore, we revealed that RRAS2 expression was mediated by H3K18la, and RRAS2 played a crucial role in HNSCC malignant progression. Moreover, high expression of RRAS2 might activate HNSCC-associated KEGG pathways and therapy resistance. In summary, H3K18la-induced RRAS2 was associated with HNSCC prognosis, and played a crucial role in immune infiltration, chemotherapy resistance and invasion, suggesting that H3K18la-RRAS2 axis might be a novel candidate therapeutic target for HNSCC.
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