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Related Experiment Video

Updated: Jun 27, 2026

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes

Published on: February 22, 2012

HPV16 E6 oncoprotein increases cell adhesion in human keratinocytes.

Alexander Epshtein¹, A Jackman, P Gonen

¹Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. epshtein@sbcglobal.net

Archives of Virology

|December 11, 2008

Summary

Human papillomavirus (HPV) 16 E6 oncoprotein enhances cell adhesion in keratinocytes. This effect is independent of p53 targeting, suggesting alternative molecular pathways are involved in HPV-induced cell changes.

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Published on: March 11, 2014

Area of Science:

Cell Biology
Virology
Oncology

Background:

The E6 oncoprotein of human papillomavirus (HPV) 16 is known to reduce apoptosis in primary human keratinocytes (PHKs).
Increased cell adhesion has been hypothesized as a potential mechanism underlying this reduced apoptosis.

Purpose of the Study:

To investigate whether HPV16 E6 expression increases cell adhesion.
To determine the role of the p53 targeting region of E6 in mediating this effect.
To explore the molecular pathways involved in E6-mediated cell adhesion.

Main Methods:

Cell adhesion assays were performed using PHKs, HaCaT, and 293T cells seeded on poly(HEME)-coated dishes.
The E6 gene was introduced via retroviral infection or DNA transfection.
HPV16 E6 mutants were analyzed for their effect on cell adhesion in 293T cells.
Tyrosine kinase inhibition assays using bombesin were conducted.

Main Results:

Expression of HPV16 E6 significantly increased the proportion of attached cells across all cell types tested.
Mutational analysis revealed that the p53-binding domain of E6 is dispensable for enhancing cell adhesion.
Inhibition of tyrosine kinases by bombesin suggests E6 may employ alternative signaling pathways to modulate cell adhesion.

Conclusions:

HPV16 E6 expression enhances cell adhesion in human keratinocytes and other cell lines.
The mechanism by which E6 increases cell adhesion does not rely on its ability to target p53.
Alternative signaling pathways, potentially involving tyrosine kinases, are likely responsible for E6-mediated cell adhesion modulation.