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Buitrago-Pérez A, Garaulet G, Vázquez-Carballo A, et al. Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling. Curr Genomics. 2009;10(1):26-34doi: 10.2174/138920209787581235.
Buitrago-Pérez, A., Garaulet, G., Vázquez-Carballo, A., Paramio, J. M., & García-Escudero, R. (2009). Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling. Current genomics, 10(1), 26-34. https://doi.org/10.2174/138920209787581235
Buitrago-Pérez, Agueda, et al. "Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling." Current genomics vol. 10,1 (2009): 26-34. doi: https://doi.org/10.2174/138920209787581235
Buitrago-Pérez A, Garaulet G, Vázquez-Carballo A, Paramio JM, García-Escudero R. Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling. Curr Genomics. 2009 Mar;10(1):26-34. doi: 10.2174/138920209787581235. PMID: 19721808; PMCID: PMC2699838.
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Curr Genomics. 2009 Mar;10(1):26-34. doi: 10.2174/138920209787581235.

Molecular Signature of HPV-Induced Carcinogenesis: pRb, p53 and Gene Expression Profiling.

Current genomics

Agueda Buitrago-Pérez, Guillermo Garaulet, Ana Vázquez-Carballo, Jesús M Paramio, Ramón García-Escudero

Affiliations

  1. Molecular Oncology Unit, Molecular Biomedicine Division, CIEMAT, Ave. Complutense 22, E-28040 Madrid, Spain.

PMID: 19721808 PMCID: PMC2699838 DOI: 10.2174/138920209787581235

Abstract

The infection by mucosal human papillomavirus (HPV) is causally associated with tumor development in cervix and oropharynx. The mechanisms responsible for this oncogenic potential are mainly due to the product activities of two early viral oncogenes: E6 and E7. Although a large number of cellular targets have been described for both oncoproteins, the interaction with tumor suppressors p53 and retinoblastoma protein (pRb) emerged as the key functional activities. E6 degrades tumor suppressor p53, thus inhibiting p53-dependent functions, whereas E7 binds and degrades pRb, allowing the transcription of E2F-dependent genes. Since these two tumor suppressors exert their actions through transcriptional modulation, functional genomics has provided a large body of data that reflects the altered gene expression of HPVinfected cells or tissues. Here we will review the similarities and differences of these findings, and we also compare them with those obtained with transgenic mouse models bearing the deletion of some of the viral oncogene targets. The comparative analysis supports molecular evidences about the role of oncogenes E6 and E7 in the interference with the mentioned cellular functions, and also suggests that the mentioned transgenic mice can be used as models for HPV-associated diseases such as human cervical, oropharynx, and skin carcinomas.

Keywords: E6; E7; Human papillomavirus; cervical cancer; gene expression profiling; oropharyngeal cancer; p53.; pRb

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