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

Viruses

Leslie Olmedo-Nieva¹  Marcela Lizano¹  Adriana Contreras-Paredes¹  J. Omar Muñoz-Bello¹ 

[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;

关键词: HPV;    E6;    splicing;    E6*;    spliceosome;   

DOI  :  10.3390/v10010045

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown