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<p>The key carcinogenic factor for nasopharyngeal cancer (NPC) is infection with the Epstein-Barr virus (EBV), significantly contributing to its occurrence and development. Insulin-like growth factor binding protein 2 (IGFBP2), known for its aberrant expression in various cancers, plays a pivotal role in oncogenic networks. Investigating IGFBP2's function and mechanism in EBV-associated NPC was the goal of the current study. The findings indicated that IGFBP2 expression was markedly higher in EBV-positive NPC cells compared to EBV-negative NPC cells, and EBV could up-regulate IGFBP2 expression by activating the TGF-β pathway through its encoded EBNA1. Furthermore, IGFBP2 influenced key carcinogenic processes, including proliferation, migration, epithelial-mesenchymal transition (EMT), and cell cycle progression in NPC cells. Notably, knockdown of IGFBP2 in the EBV-infected epithelial cell line C666-1 led to a reduction in the expression of EBV-encoded latent and lytic phase gene proteins, as well as a decrease in the copy number of the EBV genome. These results point to a reciprocal regulation link between EBV and IGFBP2, opening up a promising avenue for future clinical treatment and experimental research.</p>

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IGFBP2 up-regulation by EBV via TGF-β signaling: a key mechanism in nasopharyngeal carcinoma progression

  • 期刊论文

  • 发表日期：

    2025年7月15日

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  • Mengwen Lv,
  • Duo Shi,
  • Xia Zhao,
  • Yan Zhang,
  • Wen Liu,
  • Shuzhen Liu

摘要

The key carcinogenic factor for nasopharyngeal cancer (NPC) is infection with the Epstein-Barr virus (EBV), significantly contributing to its occurrence and development. Insulin-like growth factor binding protein 2 (IGFBP2), known for its aberrant expression in various cancers, plays a pivotal role in oncogenic networks. Investigating IGFBP2's function and mechanism in EBV-associated NPC was the goal of the current study. The findings indicated that IGFBP2 expression was markedly higher in EBV-positive NPC cells compared to EBV-negative NPC cells, and EBV could up-regulate IGFBP2 expression by activating the TGF-β pathway through its encoded EBNA1. Furthermore, IGFBP2 influenced key carcinogenic processes, including proliferation, migration, epithelial-mesenchymal transition (EMT), and cell cycle progression in NPC cells. Notably, knockdown of IGFBP2 in the EBV-infected epithelial cell line C666-1 led to a reduction in the expression of EBV-encoded latent and lytic phase gene proteins, as well as a decrease in the copy number of the EBV genome. These results point to a reciprocal regulation link between EBV and IGFBP2, opening up a promising avenue for future clinical treatment and experimental research.