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Comparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism

Philippe Paget-Bailly1,2, Koceila Meznad1,2, Diane Bruyère3

  • 1EA3181, LabEx LipSTIC ANR-11-LABX-0021, UFR Santé, 19 rue Ambroise Paré, Besançon, France.

Scientific Reports
|April 13, 2019
PubMed

Insights

The Human Papillomavirus E6*I protein increases reactive oxygen species (ROS) independently of the E6 protein. E6 can counteract E6*I

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • High-risk Human Papillomavirus (HPV) infections cause anogenital and oropharyngeal cancers.
  • Alternative splicing of HPV16 transcripts generates E6 and truncated E6* isoforms, with E6*I being abundant in HPV-related cancers.
  • The specific function of the E6*I isoform remains unclear.

Purpose of the Study:

  • To investigate the biological function of the HPV16 E6*I isoform.
  • To identify cellular targets regulated by E6*I.
  • To determine the interplay between E6 and E6*I in regulating cellular processes like ROS metabolism.

Main Methods:

  • RNA sequencing to identify cellular targets deregulated by E6*I.
  • Cell culture models overexpressing E6 and/or E6*I.
  • Measurement of reactive oxygen species (ROS) levels.
  • Analysis of specific gene expression (CCL2, RAC2).

Main Results:

  • E6*I overexpression leads to increased ROS levels.
  • E6*I deregulates genes involved in ROS metabolism, including CCL2 and RAC2.
  • E6 expression counteracts the effects of E6*I on ROS production and target gene expression.
  • Co-overexpression of E6 and E6*I does not affect ROS production.

Conclusions:

  • E6*I acts independently of E6 to increase ROS production.
  • E6 can abrogate the effects of E6*I, suggesting a complex regulatory relationship.
  • The independent function of E6*I warrants further investigation in HPV16 pathogenesis.

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