ArticleAmerican journal of cancer research2025
Epigenetic regulation and tumor suppressive function of lncRNA EP300-AS1 in nasopharyngeal carcinoma through activation of TFAP2C binding to CST6: implications for diagnosis, prognosis, and therapy.
Article in American journal of cancer research, 2025. 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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Who cites it
4 citing papers in PubMed.
- Research progress on the biological function and molecular mechanism of GDF-15 in solid malignant tumors.World journal of surgical oncology · 2026Review
- Dynamic tumor microenvironment remodeling in cancer therapy resistance: molecular mechanisms and translational opportunities.Frontiers in cell and developmental biology · 2026Review
- Research on the role and mechanisms of Cystatin 6 in disease pathosis and development.Frontiers in molecular biosciences · 2026Review
- Epigenetics: the master switch of nasopharyngeal carcinoma invasion and metastasis.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
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Abstract
The long non-coding RNA EP300-AS1 (lncRNA EP300-AS1), identified as a potential regulatory factor in various cancers, remains underexplored in nasopharyngeal carcinoma (NPC). This study investigated EP300-AS1's regulatory mechanisms in NPC, particularly its interaction with transcription factor AP-2 Gamma (TFAP2C) and its effect on cystatin E/M (CST6) expression. Employing clinical samples and NPC cell lines, we conducted in vitro and in vivo xenograft experiments to assess the impacts of modulating EP300-AS1 expression. Techniques such as CCK8, migration, scratch, apoptosis assays, cell cycle analysis, immunoblotting, and fluorescence experiments elucidated EP300-AS1's role in NPC. The interaction between EP300-AS1 and TFAP2C in regulating CST6 expression was verified using FISH, ChIP, RNA pull-down, and silver staining assays. Results indicated lower expression levels of EP300-AS1 and CST6 in NPC, with EP300-AS1 suppression inhibiting cell proliferation, migration, and invasion, while promoting apoptosis and maintaining the cell cycle in the G1 phase. EP300-AS1 also modulated epithelial-mesenchymal transition (EMT) marker expression, suggesting a role in metastasis control. Conclusively, EP300-AS1 acts as a potential tumor suppressor in NPC by interacting with TFAP2C and targeting CST6, offering novel biomarkers and therapeutic targets through its influence on methylation and the tumor microenvironment.
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