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<p>Epstein-Barr virus (EBV) is a well-established oncogenic virus strongly associated with the development of nasopharyngeal carcinoma (NPC). Recent studies in transcriptomics have highlighted the crucial role of competing endogenous RNA (ceRNA) networks, including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNA (lncRNA) in NPC progression. In particular, circRNAs act as miRNA sponges, preventing them from targeting specific mRNAs and thereby altering key oncogenic pathways. EBV employs multiple mechanisms to interfere with the host’s gene regulation, alters the expression of non-coding RNAs, and introduces its own viral RNAs. These changes disrupt tumor-suppressive ceRNA axes and establish oncogenic ceRNA networks, particularly those involved in immune evasion and cell cycle progression. Despite recent advances, the precise mechanisms by which EBV manipulates ceRNA networks remain underexplored. This review synthesizes these findings to propose a framework of patterns by which EBV systematically rewires the host ceRNA network, focusing on how EBV-encoded RNAs and host non-coding RNAs contribute to tumorigenesis.</p>

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EBV-Mediated Rewiring of ceRNA Networks in Nasopharyngeal Carcinoma: Mechanisms, ncRNA Interplay, and Oncogenic Implications

  • 期刊论文

  • 发表日期：

    2025年12月3日

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  • Navaneetha Krishnan Kottairajan,
  • Sethu Thakachy Subha,
  • Zuraini Mohammad Nasir,
  • Fauzah Abd Ghani,
  • Karuppiah Thilakavathy

摘要

Epstein-Barr virus (EBV) is a well-established oncogenic virus strongly associated with the development of nasopharyngeal carcinoma (NPC). Recent studies in transcriptomics have highlighted the crucial role of competing endogenous RNA (ceRNA) networks, including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNA (lncRNA) in NPC progression. In particular, circRNAs act as miRNA sponges, preventing them from targeting specific mRNAs and thereby altering key oncogenic pathways. EBV employs multiple mechanisms to interfere with the host’s gene regulation, alters the expression of non-coding RNAs, and introduces its own viral RNAs. These changes disrupt tumor-suppressive ceRNA axes and establish oncogenic ceRNA networks, particularly those involved in immune evasion and cell cycle progression. Despite recent advances, the precise mechanisms by which EBV manipulates ceRNA networks remain underexplored. This review synthesizes these findings to propose a framework of patterns by which EBV systematically rewires the host ceRNA network, focusing on how EBV-encoded RNAs and host non-coding RNAs contribute to tumorigenesis.