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Objective <p>To investigate the role of EBV-miR-BART17-5p in promoting nasopharyngeal carcinoma (NPC) cell dedifferentiation, and to define the potential mediating function of ARID1A in this oncogenic pathway.</p> Methods <p>Based on clinical NPC specimens, we analyzed EBV-miR-BART17-5p expression via qRT-PCR and its clinicopathological correlation. In vitro, lentiviral transduction was used to establish stable overexpression models in CNE1/CNE2 cells. Functional assays (CCK-8, colony formation, Transwell, tumor-sphere formation) and molecular analyses (Western blot, qRT-PCR) were performed. The targeting relationship was validated using dual-luciferase reporter assays. Immunohistochemistry assessed ARID1A and differentiation markers expression in tissue microarrays.</p> Results <p>EBV-miR-BART17-5p expression was elevated in advanced-stage and undifferentiated NPC tissues and correlated with poor patient prognosis. Functionally, it promoted NPC cell proliferation, migration, invasion, tumor-sphere formation, and induced dedifferentiation and stem-like phenotypes. Mechanistically, EBV-miR-BART17-5p directly targeted and downregulated ARID1A, whose low expression was similarly associated with advanced disease, poor survival, and a dedifferentiated phenotype. Crucially, ARID1A overexpression partially rescued the dedifferentiation effects induced by EBV-miR-BART17-5p.</p> Conclusion <p>This study reveals that EBV-miR-BART17-5p promotes NPC dedifferentiation and malignant progression by targeting ARID1A, identifying a novel viral miRNA tumor-suppressor axis with therapeutic potential.</p>

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Research on EBV-miR-BART17-5p targeted Inhibition of ARID1A expression to regulate nasopharyngeal carcinoma dedifferentiation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月14日

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  • Zhen Wu,
  • Xinxiang Su,
  • Yaping Qin ,
  • Junjun Pu,
  • Shengjun Xiao,
  • Xiaoling Zhang

摘要

Objective

To investigate the role of EBV-miR-BART17-5p in promoting nasopharyngeal carcinoma (NPC) cell dedifferentiation, and to define the potential mediating function of ARID1A in this oncogenic pathway.

Methods

Based on clinical NPC specimens, we analyzed EBV-miR-BART17-5p expression via qRT-PCR and its clinicopathological correlation. In vitro, lentiviral transduction was used to establish stable overexpression models in CNE1/CNE2 cells. Functional assays (CCK-8, colony formation, Transwell, tumor-sphere formation) and molecular analyses (Western blot, qRT-PCR) were performed. The targeting relationship was validated using dual-luciferase reporter assays. Immunohistochemistry assessed ARID1A and differentiation markers expression in tissue microarrays.

Results

EBV-miR-BART17-5p expression was elevated in advanced-stage and undifferentiated NPC tissues and correlated with poor patient prognosis. Functionally, it promoted NPC cell proliferation, migration, invasion, tumor-sphere formation, and induced dedifferentiation and stem-like phenotypes. Mechanistically, EBV-miR-BART17-5p directly targeted and downregulated ARID1A, whose low expression was similarly associated with advanced disease, poor survival, and a dedifferentiated phenotype. Crucially, ARID1A overexpression partially rescued the dedifferentiation effects induced by EBV-miR-BART17-5p.

Conclusion

This study reveals that EBV-miR-BART17-5p promotes NPC dedifferentiation and malignant progression by targeting ARID1A, identifying a novel viral miRNA tumor-suppressor axis with therapeutic potential.