4.6 Review

Post-Transcriptional Gene Regulation by HPV 16E6 and Its Host Protein Partners

期刊

VIRUSES-BASEL
卷 14, 期 7, 页码 -

出版社

MDPI
DOI: 10.3390/v14071483

关键词

human papillomavirus; E6; NFX1-123; PABPCs; RNA regulation; cervical cancer; hTERT

类别

资金

  1. National Institutes of Health (NIH) [R01 CA172742]
  2. NIH [R01 CA172742]

向作者/读者索取更多资源

HPV 16, the most common oncogenic type of HPV, has a protein, E6, that disrupts normal cellular processes by binding cellular proteins and regulating gene expression; recent studies have found that 16E6 can also post-transcriptionally regulate cellular genes and pathways by binding cellular RNA processing and binding proteins, offering new insights for therapeutic strategies in HPV-associated cancers.
Human papillomavirus type 16 (HPV 16) is the most common oncogenic type of HPV in cervical, anogenital, and head and neck cancers, making HPV 16 an important high-risk HPV (HR HPV) type. To create an environment permissible for viral maintenance and growth and to initiate and support oncogenesis, the HR HPV protein E6 functions to dysregulate normal cellular processes. HR HPV type 16 E6 (16E6) has previously been shown to bind cellular proteins in order to transcriptionally activate genes and to target regulatory proteins for degradation. We have identified an additional functional model for 16E6. First, 16E6 binds to cellular RNA processing and binding proteins, specifically cytoplasmic poly(A) binding proteins (PABPCs) and NFX1-123. Then, 16E6 hijacks those proteins' functions to post-transcriptionally regulate cellular immortalization, growth, and differentiation genes and pathways in keratinocytes. In this review, we have highlighted studies that introduce this new model of 16E6 functionality. Understanding ways in which HR HPV dysregulates cellular processes-particularly at the level of post-transcriptional gene regulation-presents new ways to consider mechanisms underlying DNA tumor virus function and new areas for therapeutic target development in HPV-associated cancers.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据