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p53-dependent R-loop formation and HPV pathogenesis.

Conor Winslow Templeton1, Laimonis A Laimins1

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Proceedings of the National Academy of Sciences of the United States of America
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Summary
This summary is machine-generated.

High levels of R-loops (RNA:DNA hybrids) are critical for high-risk human papillomavirus (HPV) survival and cancer development. Suppressing the p53 pathway by the E6 oncoprotein drives R-loop accumulation, promoting genomic instability.

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HPVR-loopslife cyclep53

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Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • R-loops (RNA:DNA hybrids) regulate transcription but aberrant formation causes genomic instability.
  • High-risk human papillomaviruses (HPV) are linked to cancers and increased DNA breaks.

Purpose of the Study:

  • To investigate the role of R-loops in HPV pathogenesis.
  • To determine the mechanism by which HPV induces R-loop accumulation.
  • To explore R-loops as a therapeutic target in HPV-driven cancers.

Main Methods:

  • Quantification of R-loop levels in HPV-positive and normal cells.
  • Analysis of RNase H1's role in R-loop resolution.
  • Investigating the impact of R-loop modulation on viral replication and DNA repair pathways.
  • Assessing the role of the HPV E6 oncoprotein and p53 pathway.

Main Results:

  • R-loop levels were up to 50-fold higher in HPV-positive cells and cervical carcinomas.
  • RNase H1 depletion exacerbated R-loops, impairing viral functions and DNA repair gene expression.
  • RNase H1 overexpression reduced R-loops and DNA breaks but blocked viral replication.
  • HPV E6 oncoprotein induced R-loops by inhibiting p53 transcriptional activity.

Conclusions:

  • Elevated R-loop levels are essential for the HPV life cycle and pathogenesis.
  • HPV maintains high R-loop levels by suppressing the p53 pathway.
  • Targeting R-loop resolution may offer a therapeutic strategy against HPV-driven cancers.