Abstract
Human papillomavirus (HPV) E6 and E7 oncoproteins are critical for development and maintenance of the malignant phenotype in HPV-induced cancers. These two viral oncoproteins interfere with a plethora of cellular pathways, including the regulation of cell cycle and the control of apoptosis, which are critical in maintaining normal cellular functions. E6 and E7 bind directly with certain components of the Ubiquitin Proteasome System (UPS), enabling them to manipulate a number of important cellular pathways. These activities are the means by which HPV establishes an environment supporting the normal viral life cycle, however in some instances they can also lead to the development of malignancy. In this review, we have discussed how E6 and E7 oncoproteins from alpha and beta HPV types interact with the components of the UPS, and how this interplay contributes to the development of cancer.
Highlights
Papillomaviridae is a diverse family of small, non-enveloped DNA viruses, approximately 50–60 nm in diameter that infect all homoeothermic vertebrates including humans [1,2]
The interplay between E6/E7 oncoproteins from various Human papillomavirus (HPV) types and the Ubiquitin Proteasome System (UPS) has been shown to be one of the critical strategies used by these viruses to create an optimal environment in which they can successfully replicate
E6/E7 from β-HPVs, which are characterized as co-factors in causing skin cancers under specific conditions, interact with significantly fewer components of the UPS, while E6/E7 from LR types interact with only a few components of the UPS
Summary
Papillomaviridae is a diverse family of small, non-enveloped DNA viruses, approximately 50–60 nm in diameter that infect all homoeothermic vertebrates including humans [1,2]. Β-HPVs are primarily considered to be non-carcinogenic in the general population, some β-HPV types, such as HPV-5 and HPV-8, can represent a potential cancer risk in particular hypersensitive groups (e.g., in cases of severe immunodeficiency and in epidermodysplasia verruciformis patients), where β-HPVs have been found in skin warts and in cutaneous squamous cell carcinomas (CSCC) [17,18]. These β-HPVs are characterized as co-factors, which, in combination with ultraviolet (UV) irradiation, have been thought to contribute to the development of non-melanoma skin cancers (NMSC) [16]. Studies have demonstrated that the process of viral integration is absent during β-HPV infections and there is no requirement for continual oncoprotein expression to allow the persistence of the transformed phenotype during CSCC, indicating that β-HPVs contribute to the initial steps of tumor formation, but are not necessary for its continued maintenance [16,17,28,30,31]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
