Título del libro: Cervical Cancer
Título del capítulo: Malignant transforming mechanisms of human papillomavirus
LUIS SOTERO BENITEZ Y BRIBIESCA;
Autores externos:
Idioma:
Inglés
Año de publicación:
2017
Palabras clave:
C-myc; Dysbiosis; E6; E7; High risk-HPV; HPV; HPV genome integration; Neoplastic transformation; Oncobioma; P53; PRb; Telomerase; Tumor metabolome
Resumen:
HPVs transforming activities represent the viral replication strategy that is driven to replicate viral genomes and to establish long-term maintenance in a tissue. High-risk-HPV-infected cells and carcinogenesis progression are terminal events, since cancer cells contain integrated HPV genomes and do produce viral progeny. High-risk HPV (HR-HPV) genome integration indeed represents a consequence of HPV E6/E7- induced genomic instability. HR-HPV E6 and E7 proteins critically contribute to viral life cycle and transforming activity. HR-HPV E7 proteins bind to pRB and decreased efficiency. HR-HPV E6 proteins efficiently interact with TP53 and promote for TP53 degradation. High-risk HPVs can frequently persist for decades in an infected host cell at a low number of copies. One of the events of HPVinduced carcinogenesis is the HPV genome integration into a host chromosome, and it is probably a failed viral mechanism. High Risk-HPV E6 proteins and E7 contribute to immortalization of primary human epithelial cells by induction of telomerase activity. Data evidences suggest that microbial dysbiosis is associated with malignant transformation, but future discussion and direction for microbiome in cancer research (oncobioma) and particularly in HPV-associated human cancer could be evaluated as causative causes that modulate initiation, progression, or cancer metastasis. © Springer International Publishing Switzerland 2017.
Entidades citadas de la UNAM:
ISBN:
9783319452319
Editorial:
Springer International Publishing Nombre de la publicación:
Malignant transforming mechanisms of human papillomavirus
Página inicial:
35
Página final:
56
