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Viruses 2018, 10(1), 45; doi:10.3390/v10010045

The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis

1
Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, México/Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Av. San Fernando No. 22, Col. Sección XVI, Tlalpan, 14080 Mexico City, Mexico
2
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico
*
Author to whom correspondence should be addressed.
Received: 22 December 2017 / Revised: 12 January 2018 / Accepted: 15 January 2018 / Published: 18 January 2018
(This article belongs to the Section Animal Viruses)
View Full-Text   |   Download PDF [1937 KB, uploaded 18 January 2018]   |  

Abstract

Persistent infections with High Risk Human Papillomaviruses (HR-HPVs) are the main cause of cervical cancer development. The E6 and E7 oncoproteins of HR-HPVs are derived from a polycistronic pre-mRNA transcribed from an HPV early promoter. Through alternative splicing, this pre-mRNA produces a variety of E6 spliced transcripts termed E6*. In pre-malignant lesions and HPV-related cancers, different E6/E6* transcriptional patterns have been found, although they have not been clearly associated to cancer development. Moreover, there is a controversy about the participation of E6* proteins in cancer progression. This review addresses the regulation of E6 splicing and the different functions that have been found for E6* proteins, as well as their possible role in HPV-induced carcinogenesis. View Full-Text
Keywords: HPV; E6; splicing; E6*; spliceosome HPV; E6; splicing; E6*; spliceosome
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Olmedo-Nieva, L.; Muñoz-Bello, J.O.; Contreras-Paredes, A.; Lizano, M. The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis. Viruses 2018, 10, 45.

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