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Viruses 2018, 10(1), 45;

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

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
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)
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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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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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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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