Human papillomavirus E6 and E7 oncoproteins as risk factors for tumorigenesis

  title={Human papillomavirus E6 and E7 oncoproteins as risk factors for tumorigenesis},
  author={Niladri Ganguly and Suraj P. Parihar},
  journal={Journal of Biosciences},
Human papillomavirus (HPV) is small, double-stranded DNA virus that infects mucosal and cutaneous epithelial tissue. HPV is sexually transmitted and the viral DNA replicates extrachromosomally. The virus is non-enveloped and has an icosahedral capsid. There are approximately 118 types of HPV, which are characterized as high-risk or lowrisk types. High-risk HPVs cause malignant transformation while the low-risk ones cause benign warts and lesions. The expression of E6 and E7 is normally… 
Human papillomavirus-16 E5 protein: oncogenic role and therapeutic value
This review attempts to discuss the positive role of HPV16 E5 in the form of therapeutic target for cervical cancer, as well as its role in modulation of several intracellular signalling pathways leading to transformed phenotype of the host cell.
Viral load and interaction of HPV oncoprotein E6 and E7 with host cellular markers in the progression of cervical cancer
Molecular pathogenesis, viral load, and the interaction of HPV oncoprotein E6 and E7 with host cellular markers in the progression of cervical cancer are reviewed.
Modulation of DNA methylation by human papillomavirus E6 and E7 oncoproteins in cervical cancer
The present review discusses how epigenetic mechanisms may be targeted for possible therapeutic interventions for HPV mediated cervical cancer.
HPV Integration in Head and Neck Squamous Cell Carcinomas: Cause and Consequence.
  • E. Speel
  • Biology, Medicine
    Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer
  • 2017
The causes and consequences of HPV Integration are summarized from the literature, with special focus on the site of HPV integration in the cellular genome, and its effect on expression of viral oncogenes, on human (tumor) gene expression and on deregulation of cell proliferation, apoptosis and cell signaling pathways.
Human Papillomavirus Type 16 E5 Protein Induces Expression of Beta Interferon through Interferon Regulatory Factor 1 in Human Keratinocytes
The data show a new and unexpected role for HR-HPV E5 protein and indicate that HPV16 E5 may contribute to the mechanisms responsible for cervical carcinogenesis in part via stimulation of IFN-β and an IFN signature, with IRF-1 playing a pivotal role.
Overexpression of HPV16 E6* Alters β-Integrin and Mitochondrial Dysfunction Pathways in Cervical Cancer Cells.
E6*, the smaller splice isoform of the E6 oncogene, modifies the expression of proteins involved in mitochondrial dysfunction and oxidative phosphorylation in C33A cells, and β-integrin signaling in SiHa cells.
Human papillomavirus E5 protein, the undercover culprit of tumorigenesis
It is suggested that the HPV E5 protein should be acknowledged as an oncoprotein of HPV and investigated for its role in cancer progression and maintenance.
Revealing highly conserved regions in the E6 protein among distinct human papillomavirus types using comparative analysis of multiple sequence alignments.
It is yet well elucidated that high risk genotypes lead to the development of cervical cancer and are also associated with other mucosal anogenital, head and neck tumors.


Expression of HPV16 E6 or E7 increases integration of foreign DNA.
At least some of the difference in oncogenic potential observed between high-risk and low-risk HPV types may be determined by the increased ability of high- risk HPVs to integrate into host DNA.
Human Papillomavirus Oncoprotein E6 Inactivates the Transcriptional Coactivator Human ADA3
Findings reveal a novel strategy of HPV E6-induced loss of p53 function that is independent of direct p53 degradation, and inactivation of its function may allow E6 to perturb numerous cellular pathways during HPV oncogenesis.
Human papillomavirus (HPV) E6 interactions with Bak are conserved amongst E6 proteins from high and low risk HPV types.
The E6 proteins from HPV-18, HPV-16 and HPV-11 can all bind to Bak in vitro, stimulate its degradation in vivo and reduce Bak-induced apoptosis, indicating that the ability of HPV to circumvent the apoptosis induced by Bak may contribute to the oncogenic potential of the virus.
The role of human papilloma virus in the molecular biology of cervical carcinogenesis.
A large body of knowledge already generated in this area supports the view that high-risk HPV types have the ability to transform cells into a malignant phenotype, but it remains unclear how and when cofactors or factors that are innate in the HPV-infected cells launch the host cells into an irreversible progression to carcinoma.
Human papillomavirus immortalization and transformation functions.
Immortalization of human cells and their malignant conversion by high risk human papillomavirus genotypes.
High risk HPV oncogenes fulfill dual functions in genome-harboring cells: their derived oncoproteins stimulate cell growth by pleiotropic effects and act as progression factors by inducing mutations in host cell DNA and aneuploidy.
The human papillomavirus E7 oncoprotein abrogates signaling mediated by interferon-alpha.
The results suggest that HPV, via E7, targets p48, resulting in the loss of IFNalpha-mediated signal transduction and may provide a means by which HPV can avoid the innate immune system.
The E6 Oncoproteins of High-Risk Papillomaviruses Bind to a Novel Putative GAP Protein, E6TP1, and Target It for Degradation
Using the yeast two-hybrid system, a novel E6-binding protein is isolated, designated E6TP1 (E6-targeted protein 1), which exhibits high homology to GTPase-activating proteins for Rap, including SPA-1, tuberin, and Rap1GAP and is a potential link between HPV E6 oncogenesis and alteration of a small G protein signaling pathway.
Papillomavirus genome structure, expression, and post-transcriptional regulation.
Continuing research on post-transcriptional regulation of papillomavirus infection will remain as a future focus to provide more insights into papillumavirus-host interactions, the virus life-cycle, and viral oncogenesis.
The human papillomavirus type 16 E6 and E7 oncoproteins independently induce numerical and structural chromosome instability.
It is reported that expression of HPV-16 E6 and E7 independently results in various mitotic abnormalities that suggest that HPV oncoproteins are a source for both numerical and structural chromosome instability during HPV-associated carcinogenesis.