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Open AccessEditor’s ChoiceReview

Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers

1
Molecular Biology and Viral Oncology Unit, Istituto Nazionale Tumori IRCCS “Fondazione G. Pascale”, via Mariano Semmola, 80131 Napoli, Italy
2
Cancer Immunomodulation Unit, Istituto Nazionale Tumori IRCCS “Fondazione G. Pascale”, via Mariano Semmola, 80131 Napoli, Italy
*
Author to whom correspondence should be addressed.
Cancers 2018, 10(7), 213; https://doi.org/10.3390/cancers10070213
Received: 5 June 2018 / Revised: 19 June 2018 / Accepted: 22 June 2018 / Published: 22 June 2018
(This article belongs to the Special Issue p53 Signaling in Cancers)
Viral oncogenesis is a multistep process largely depending on the complex interplay between viruses and host factors. The oncoviruses are capable of subverting the cell signaling machinery and metabolic pathways and exploit them for infection, replication, and persistence. Several viral oncoproteins are able to functionally inactivate the tumor suppressor p53, causing deregulated expression of many genes orchestrated by p53, such as those involved in apoptosis, DNA stability, and cell proliferation. The Epstein–Barr virus (EBV) BZLF1, the high-risk human papillomavirus (HPV) E6, and the hepatitis C virus (HCV) NS5 proteins have shown to directly bind to and degrade p53. The hepatitis B virus (HBV) HBx and the human T cell lymphotropic virus-1 (HTLV-1) Tax proteins inhibit p53 activity through the modulation of p300/CBP nuclear factors, while the Kaposi’s sarcoma herpesvirus (HHV8) LANA, vIRF-1 and vIRF-3 proteins have been shown to destabilize the oncosuppressor, causing a decrease in its levels in the infected cells. The large T antigen of the Merkel cell polyomavirus (MCPyV) does not bind to p53 but significantly reduces p53-dependent transcription. This review describes the main molecular mechanisms involved in the interaction between viral oncoproteins and p53-related pathways as well as in the development of therapeutic strategies targeting such interactions. View Full-Text
Keywords: oncoviruses; EBV; HCV; HBV; HPV; HHV-8; HTLVI; MCPyV; p53 oncoviruses; EBV; HCV; HBV; HPV; HHV-8; HTLVI; MCPyV; p53
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MDPI and ACS Style

Tornesello, M.L.; Annunziata, C.; Tornesello, A.L.; Buonaguro, L.; Buonaguro, F.M. Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers. Cancers 2018, 10, 213. https://doi.org/10.3390/cancers10070213

AMA Style

Tornesello ML, Annunziata C, Tornesello AL, Buonaguro L, Buonaguro FM. Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers. Cancers. 2018; 10(7):213. https://doi.org/10.3390/cancers10070213

Chicago/Turabian Style

Tornesello, Maria Lina; Annunziata, Clorinda; Tornesello, Anna Lucia; Buonaguro, Luigi; Buonaguro, Franco Maria. 2018. "Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers" Cancers 10, no. 7: 213. https://doi.org/10.3390/cancers10070213

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