Research Article
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Published Online: 20 September 2006

E6 and E7 Oncoproteins from Human Papillomavirus Type 16 Induce Activation of Human Transforming Growth Factor β 1 Promoter throughout Sp1 Recognition Sequence

Publication: Viral Immunology
Volume 19, Issue Number 3

Abstract

Human Papillomavirus (HPV) infection is the main etiologic agent of cervical cancer and HPV E6 and E7 oncogenes trans-regulate many cellular genes. An association between TGF-β 1 gene expression and cervical cancer development has been suggested; however, the mechanisms by which HPV influences TGF-β 1 expression remain unclear. In the present study we analyzed the mechanism through which HPV-16 E6 and E7 oncoproteins regulate the TGF-β 1 promoter in cervical tumor cells. Our results showed that E6 and E7 increased TGF-β 1 promoter activity. Furthermore, we identified a specific DNA sequence motif in the TGF-β 1 core promoter that is responsible for trans-activation and that corresponds to the Sp1e-binding site associated with HPV-16 E6 and E7 oncoproteins. Mutational analysis showed that the Sp1e recognition site abolished the trans-activation caused by E6 and E7. These results suggest a physical interaction and functional cooperation between viral oncoproteins and cellular regulatory elements of the TGF-β 1 promoter, and may explain the contribution of HPV-16 to TGF-β 1 gene expression in cervical cancer.

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Published In

cover image Viral Immunology
Viral Immunology
Volume 19Issue Number 3Fall 2006
Pages: 468 - 480
PubMed: 16987065

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Published online: 20 September 2006
Published in print: Fall 2006

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Oscar Peralta-Zaragoza
Division of Molecular Biology of Pathogens, National Institute of Public Health, Cuernavaca, Mexico.
Víctor Bermúdez-Morales
Division of Molecular Biology of Pathogens, National Institute of Public Health, Cuernavaca, Mexico.
Lourdes Gutiérrez-Xicotencatl
Division of Molecular Biology of Pathogens, National Institute of Public Health, Cuernavaca, Mexico.
Juan Alcocer-González
School of Biological Sciences, Autonomous University of Nuevo León, Monterrey, Mexico.
Félix Recillas-Targa
Department of Molecular Genetics, Institute of Cellular Physiology, National Autonomous University of Mexico, Mexico City, DF Mexico.
Dr. Vicente Madrid-Marina
Division of Molecular Biology of Pathogens, National Institute of Public Health, Cuernavaca, Mexico.

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