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Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
Published on: September 28, 2012
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Human papillomavirus E7 induces p63 expression to modulate DNA damage response.
Sahar Eldakhakhny1, Qing Zhou1, Emma J Crosbie1
1Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester Cancer Research Centre, Wilmslow Road, Manchester, M20 4QL, UK.
Cell Death & Disease
|January 28, 2018
Summary
High-risk human papillomavirus (HR-HPV) E7 protein boosts cervical cancer cell DNA repair via p63 induction. This mechanism may affect radiation therapy sensitivity in cervical cancer patients.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Cervical cancer is a global health concern, primarily caused by persistent high-risk human papillomavirus (HR-HPV) infections.
- Over 99% of cervical cancers show evidence of HR-HPV sequences, highlighting its etiological role.
Purpose of the Study:
- To elucidate a novel mechanism by which HR-HPV E7 oncoprotein influences DNA damage response in cervical cancer cells.
- To investigate the role of p63 in mediating DNA damage repair modulated by HR-HPV.
Main Methods:
- Analysis of HR-HPV E7 oncoprotein's effect on gene transcription in cervical cancer cells.
- Investigating the modulation of DNA damage response pathways.
- Assessing the role of p63 in DNA repair processes.
Main Results:
- HR-HPV E7 oncoprotein was found to induce the transcription of p63, a p53-family member.
- p63 modulates DNA damage response pathways, facilitating DNA repair in cervical cancer cells.
- A critical role for p63 in DNA damage response within cervical cancer was demonstrated.
Conclusions:
- HR-HPV E7 protein employs a mechanism involving p63 induction to enhance DNA repair in cervical cancer cells.
- This interaction suggests HR-HPV may influence the efficacy of radiation therapy by altering DNA repair efficiency.
- The study identifies p63 as a key player in the DNA damage response in the context of cervical cancer.
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