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Updated: Jun 30, 2025

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
Published on: March 8, 2012
HPV16 E7 modulates the cell surface expression of MET and CD109 via the AP2 complex
Oscar Trejo-Cerro1, Om Basukala2, Michael P Myers1
1International Centre for Genetic Engineering and Biotechnology, Padriciano 99, I-34149, Trieste, Italy.
Abstract:
Multiple cellular pathways are affected by HPV E6 and E7 oncoproteins, including endocytic and cellular trafficking. HPV-16 E7 can target the adaptor protein (AP) complex, which contains proteins important during endocytosis transport. To further investigate the role of HPV E7 during this process, we analysed the expression of cell surface proteins in NIKS cells expressing HPV-16 E7. We show that different cell surface proteins are regulated by HPV-16 E7 via interaction with AP2. We observed that the expression of MET and CD109 membrane protein seems to be upregulated in cells expressing E7. Moreover, the interaction of MET and CD109 with AP2 proteins is disrupted by HPV-16 E7. In addition, in the absence of HPV-16 E7, there is a downregulation of the cell membrane expression of MET and CD109 in HPV-positive cell lines. These results expand our knowledge of the functions of E7 and open new potential cellular pathways affected by this oncoprotein.
Insights
Human papillomavirus (HPV) oncoprotein E7 affects cell surface protein levels by interacting with the AP2 complex. HPV-16 E7 dysregulates MET and CD109 expression, impacting cellular trafficking pathways.
Area of Science:
- Molecular Biology
- Cell Biology
- Virology
Background:
- Human papillomavirus (HPV) oncoproteins E6 and E7 are key factors in cervical cancer development.
- These oncoproteins disrupt cellular pathways, including endocytic and cellular trafficking.
- HPV-16 E7 specifically targets adaptor protein (AP) complexes involved in endocytosis.
Purpose of the Study:
- To investigate the role of HPV-16 E7 in regulating cell surface protein expression.
- To determine how HPV-16 E7 interacts with the AP2 complex.
- To elucidate the impact of HPV-16 E7 on MET and CD109 membrane protein expression.
Main Methods:
- Analysis of cell surface protein expression in NIKS cells engineered to express HPV-16 E7.
- Investigating the interaction between HPV-16 E7, AP2, MET, and CD109 using cellular assays.
- Comparing protein expression in HPV-positive cell lines with and without HPV-16 E7 expression.
Main Results:
- HPV-16 E7 regulates cell surface proteins through interaction with the AP2 complex.
- MET and CD109 membrane protein expression is upregulated in cells expressing HPV-16 E7.
- HPV-16 E7 disrupts the interaction between MET, CD109, and AP2 proteins.
- Absence of HPV-16 E7 leads to downregulation of MET and CD109 in HPV-positive cell lines.
Conclusions:
- HPV-16 E7 significantly impacts cell surface protein expression and cellular trafficking.
- The interaction between HPV-16 E7 and AP2 influences the regulation of MET and CD109.
- These findings expand the understanding of HPV oncoprotein functions and identify potential therapeutic targets.
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