Abstract
Human papillomaviruses (HPVs) are small DNA viruses; some oncogenic ones can cause different types of cancer, in particular cervical cancer. HPV-associated carcinogenesis provides a classical model system for RNA interference (RNAi) based cancer therapies, because the viral oncogenes E6 and E7 that cause cervical cancer are expressed only in cancerous cells. Previous studies on the development of therapeutic RNAi facilitated the advancement of therapeutic siRNAs and demonstrated its versatility by siRNA-mediated depletion of single or multiple cellular/viral targets. Sequence-specific gene silencing using RNAi shows promise as a novel therapeutic approach for the treatment of a variety of diseases that currently lack effective treatments. However, siRNA-based targeting requires further validation of its efficacy in vitro and in vivo, for its potential off-target effects, and of the design of conventional therapies to be used in combination with siRNAs and their drug delivery vehicles. In this review we discuss what is currently known about HPV-associated carcinogenesis and the potential for combining siRNA with other treatment strategies for the development of future therapies. Finally, we present our assessment of the most promising path to the development of RNAi therapeutic strategies for clinical settings.
Highlights
Human papillomaviruses (HPVs) are small DNA viruses with a genome size ~8 kb long
Functional restoration of WT-tumor suppressor protein p53 (TP53) may induce the regression of cervical carcinomas, which can be achieved by abrogating the expression of the E6 or E6/E7 oncogenes, or through cisplatin or radiation treatment
In spite of recent progress and various treatment modalities that have proved beneficial to some extent, no effective treatment is currently available for HPV-associated carcinogenesis
Summary
Human papillomaviruses (HPVs) are small DNA viruses with a genome size ~8 kb long. They infect cutaneous or mucosal epithelial cells, genital tissues, and the upper respiratory tract. Over 200 genetically distinct subtypes of HPV have been identified, and approximately 90 genotypes have been fully characterized Among these types, the high-risk HPVs (HR-HPVs), including HPV-16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82, are associated with more than 90% of cervical cancers, and to a lesser extent with other anogenital cancers and head and neck cancers [1,2,3,4]. During the course of HPV-mediated cancer development, the viral DNAs are frequently integrated into host cell chromosomes, and the proteins encoded by the viral genes play a critical role in carcinogenesis
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