The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis
AbstractPersistent 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
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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.
Olmedo-Nieva L, Muñoz-Bello JO, Contreras-Paredes A, Lizano M. The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis. Viruses. 2018; 10(1):45.Chicago/Turabian Style
Olmedo-Nieva, Leslie; Muñoz-Bello, J. O.; Contreras-Paredes, Adriana; Lizano, Marcela. 2018. "The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis." Viruses 10, no. 1: 45.
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