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Updated: May 10, 2026

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

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Published on: July 23, 2010

The human papillomavirus-16 E7 oncoprotein exerts antiapoptotic effects via its physical interaction with the

Anna M Mileo1, Claudia Abbruzzese, Carmen Vico

  • 1Department of Development of Therapeutic Programs, Regina Elena National Cancer Institute, IRCCS, Via Elio Chianesi 53, 00144 Rome, Italy.

Carcinogenesis
|June 5, 2013
PubMed

Insights

Human papillomavirus-16 E7 oncoprotein interacts with gelsolin, disrupting actin regulation. This leads to cell cycle changes, inhibited apoptosis, and increased cell survival, promoting HPV carcinogenesis.

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • The human papillomavirus-16 E7 oncoprotein (HPV-16 E7) is crucial for HPV-related carcinogenesis.
  • HPV-16 E7's activity relies on physical interactions with host cell targets.
  • Understanding these interactions is key to developing targeted therapies.

Purpose of the Study:

  • To identify novel cellular partners of the HPV-16 E7 oncoprotein.
  • To investigate the functional consequences of the interaction between HPV-16 E7 and its cellular partners.
  • To explore potential therapeutic strategies targeting HPV-16 E7-host cell interactions.

Main Methods:

  • Biochemical analyses to confirm protein interactions.
  • 3D molecular modeling to visualize the interaction interface.
  • Site-directed mutagenesis using specific HPV-16 E7 mutants.
  • Functional assays in human immortalized keratinocytes to assess cellular changes.

Main Results:

  • Gelsolin (GSN), an actin-binding protein, was identified as a novel binding partner for HPV-16 E7.
  • HPV-16 E7 directly affects GSN integrity and function.
  • Stable HPV-16 E7 expression leads to actin polymerization, cell cycle progression (increased S phase), apoptosis inhibition, and enhanced cell survival.

Conclusions:

  • The interaction between HPV-16 E7 and GSN disrupts normal actin dynamics, contributing to cellular reprogramming in HPV infection.
  • These findings support the development of small molecules targeting HPV-16 E7-expressing cells to hinder HPV-induced carcinogenesis.

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