Journal Article

Effects of HPV-16 E5, E6 and E7 proteins on survival, adhesion, migration and invasion of trophoblastic cells

Selma Boulenouar, Christine Weyn, Melody Van Noppen, Mohamed Moussa Ali, Michel Favre, Philippe O. Delvenne, Françoise Bex, Agnès Noël, Yvon Englert and Véronique Fontaine

in Carcinogenesis

Volume 31, issue 3, pages 473-480
Published in print March 2010 | ISSN: 0143-3334
Published online November 2009 | e-ISSN: 1460-2180 | DOI:
Effects of HPV-16 E5, E6 and E7 proteins on survival, adhesion, migration and invasion of trophoblastic cells

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics


Show Summary Details


Among high-risk human papillomaviruses (HPV), HPV-16 infection is the most prevalent causative factor for cervical cancer. Beside other mucosal targets, HPV-16 was reported to infect the placenta and to replicate in trophoblastic cells. Since these cells share invasive properties of tumoral cells, they represent an ideal model to investigate several oncogenic processes. In the present work, we analyzed the impacts of HPV-16 E5, E6 and E7 oncoproteins on the trophoblastic model. Our results showed that E5 impaired the viability of trophoblastic and cervical cell lines but E6 and E7, favoring cell growth, neutralized the E5 cytotoxic effect. In addition, E5 decreased the adhesiveness of trophoblastic cells to the tissue culture plastic and to endometrial cells similarly as described previously for E6 and E7. E5 and E6 plus E7 increased also their migration and their invasive properties. Cells expressing HPV-16 early proteins under the control of the long control region endogenous promoter displayed growth advantage and were also more motile and invasive compared with control cells. Interestingly, the E-cadherin was downregulated in trophoblastic cells expressing E5, E6 and E7. Nuclear factor-kappaB and activator protein-1 activities were also enhanced. In conclusion, HPV-16 early proteins enhanced trophoblastic growth and intensify the malignant phenotype by impairing cell adhesion leading to increased cellular motile and invasive properties. HPV-16 E5 participated, with E6 and E7, in these changes by impairing E-cadherin expression, a hallmark of malignant progression.

Journal Article.  6442 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.