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The exon junction complex core factor eIF4A3 is a key regulator of HPV16 gene expression
Koceila Meznad1,2, Philippe Paget-Bailly1,2,3, Elise Jacquin1,4
1Université Bourgogne Franche Comté, France.
Bioscience Reports
|March 24, 2021
Summary
Investigating the eukaryotic translation initiation factor 4A3 (eIF4A3) and nonsense-mediated RNA decay (NMD) in HPV16 gene expression, this study found that eIF4A3 depletion and NMD inhibition increase viral oncoprotein levels, suggesting NMD
Area of Science:
- Molecular Biology
- Virology
- Cancer Research
Background:
- High-risk human papillomaviruses (hrHPVs) cause various cancers, including ano-genital cancers and head and neck squamous cell carcinomas (HNSCCs).
- Viral oncoproteins E6 and E7 are key drivers of hrHPV-induced carcinogenesis, with their expression tightly regulated.
- The Exon Junction Complex (EJC) factor, eukaryotic translation initiation factor 4A3 (eIF4A3), plays a role in gene expression regulation.
Purpose of the Study:
- To investigate the role of eIF4A3 in the regulation of HPV16 gene expression.
- To explore the involvement of the nonsense-mediated RNA decay (NMD) pathway in controlling HPV16 oncoprotein levels.
Main Methods:
- Depletion of eIF4A3 in relevant cellular models.
- Inhibition of the nonsense-mediated RNA decay (NMD) pathway.
- Analysis of HPV16 E7 oncoprotein RNA and protein levels.
Main Results:
- Depletion of eIF4A3 led to an up-regulation of HPV16 E7 oncoprotein.
- Inhibition of the NMD pathway resulted in increased E7 RNA and protein levels.
- These findings suggest differential susceptibility of HPV16 transcripts to NMD.
Conclusions:
- The NMD pathway plays a crucial role in regulating the expression levels of HPV16 oncoproteins.
- eIF4A3 may influence HPV16 gene expression through its interaction with or regulation of the NMD pathway.
- Understanding these regulatory mechanisms could offer new insights into HPV-related cancer development and potential therapeutic strategies.
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