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Activation of Wnt Signaling Pathway by Human Papillomavirus E6 and E7 Oncogenes in HPV16-Positive Oropharyngeal Squamous Carcinoma Cells

Rampias, Theodore, Boutati, Eleni, Pectasides, Eirini, Sasaki, Clarence, Kountourakis, Panteleimon, Weinberger, Paul, Psyrri, Amanda·2010·Molecular Cancer Research
DOI 10.1158/1541-7786.mcr-09-0345

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Abstract

We sought to determine the role of human papillomavirus (HPV) E6 and E7 oncogenes in nuclear β-catenin accumulation, a hallmark of activated canonical Wnt signaling pathway. We used HPV16-positive oropharyngeal cancer cell lines 147T and 090, HPV-negative cell line 040T, and cervical cell lines SiHa (bearing integrated HPV16) and HeLa (bearing integrated HPV18) to measure the cytoplasmic and nuclear β-catenin levels and the β-catenin/Tcf transcriptional activity before and after E6/E7 gene silencing. Repression of HPV E6 and E7 genes induced a substantial reduction in nuclear β-catenin levels. Luciferase assay showed that transcriptional activation of Tcf promoter by β-catenin was lower after silencing. The protein levels of β-catenin are tightly regulated by the ubiquitin/proteasome system. We therefore performed expression analysis of regulators of β-catenin degradation and nuclear transport and showed that seven in absentia homologue (Siah-1) mRNA and protein levels were substantially upregulated after E6/E7 repression. Siah-1 protein promotes the degradation of β-catenin through the ubiquitin/proteasome system. To determine whether Siah-1 is important for the proteasomal degradation of β-catenin in HPV16-positive oropharyngeal cancer cells, we introduced a Siah-1 expression vector into 147T and 090 cells and found substantial reduction of endogenous β-catenin in these cells. Thus, E6 and E7 are involved in β-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers. In addition, we show the significance of the endogenous Siah-1–dependent ubiquitin/proteasome pathway for β-catenin degradation and its regulation by E6/E7 viral oncoproteins in HPV16-positive oropharyngeal cancer cells. Mol Cancer Res; 8(3); 433–43

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Cited by

Metadata

Authors
Rampias, T., Boutati, E., Pectasides, E., Sasaki, C., Kountourakis, P., Weinberger, P., & Psyrri, A.
Affiliations
Authors' Affiliations: Departments of 1Internal Medicine, Section of Medical Oncology, and 2Surgery, Section of Otolaryngology, Yale University School of Medicine, New Haven, Connecticut; and 3Medical School, Athens University, Athens, Greece
Venue
Molecular Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2010-03-16
Volume
8
Issue
3
Pages
433-443
ISSN
  • 1541-7786
  • 1557-3125
DOI
10.1158/1541-7786.mcr-09-0345
Cited by
105
References
3
Language
en

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