Human papillomavirus molecular biology

Harden, Mallory E.; Münger, Karl

doi:10.1016/j.mrrev.2016.07.002

Cited by 180 publications

(202 citation statements)

References 130 publications

(136 reference statements)

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“…E4 binds to cytokeratin filaments, disrupting their structure, and is thought to play a role in viral escape from the desquamated epithelium (for review see ref. ).…”

Section: Hpv Infectionmentioning

confidence: 97%

“…The ancient papillomaviruses with mucosal tropism started developing some 90 million years ago . During their evolution, human papillomaviruses (HPVs) developed, acquiring the capacity to utilize human cellular proteins for replication and to remain silent by hijacking the cellular and immune systems at several levels . The manifestations of HPV infections can be multiple, varying from asymptomatic infections to benign warty or potentially malignant lesions, intraepithelial neoplasia, and invasive carcinomas .…”

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confidence: 99%

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Oral manifestations of human papillomavirus infections

Syrjänen

2018

European J Oral Sciences

125

144

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Papillomaviruses are one of the oldest viruses known, dating back 330 million years. During this long evolution, human papillomaviruses (HPV) have developed into hijackers of human cellular and immune systems in which they replicate and remain silent. Systematic studies on oral HPV infections and their outcomes are still scarce. Oral HPV infections have been linked to sexual behaviour, but recent evidence supports their horizontal, mouth‐to‐mouth, transmission. Most HPV infections in infants are acquired vertically from the mother during the intrauterine period, during delivery, or later via saliva. The best‐known benign clinical manifestations of HPV infection are oral papilloma/condyloma and focal epithelial hyperplasia. Evidence is emerging which suggests that some oral HPV infections might persist. Persistent HPV infection is mandatory for HPV‐associated malignant transformation. However, progression of HPV‐induced lesions to malignancy requires additional cofactors. In the early 1980s, we provided the first evidence that a subset of oral cancers and other head and neck cancers might be causally linked to HPV infection. This review summarizes current knowledge on the virus itself, its transmission modes, as well as the full spectrum of oral HPV infections – from asymptomatic infections to benign, potentially malignant oral lesions, and squamous cell carcinoma.

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“…E4 binds to cytokeratin filaments, disrupting their structure, and is thought to play a role in viral escape from the desquamated epithelium (for review see ref. ).…”

Section: Hpv Infectionmentioning

confidence: 97%

mentioning

confidence: 99%

Oral manifestations of human papillomavirus infections

Syrjänen

2018

European J Oral Sciences

125

144

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“…to keep infected epithelial cells in a replication-competent state while they are differentiating. Not surprisingly, this behavior, as well as expression of the E7 oncogene, are sensed as abnormal, and the cell responds by triggering apoptosis and oncogene-induced senescence [81,82]. In fact, the high-risk HPVs have evolved to target p53 and RB1 and thus cause cancer hallmarks because p53 and RB1 are key mediators of apoptosis and senescence [83].…”

Section: The Connection Between Persistent Infection and Oncogenesismentioning

confidence: 99%

More than just oncogenes: mechanisms of tumorigenesis by human viruses

Gaglia

Münger

2018

Current Opinion in Virology

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Most humans are infected with at least one of the known human cancer viruses during their lifetimes. While the initial infection with these viruses does not cause major disease, infected cells can acquire cancer hallmarks, particularly upon immunosuppression or exposure to co-carcinogenic stimuli. Even though cancer formation represents a rare outcome of a viral infection, approximately one out of eight human cancers has a viral etiology. Viral cancers present unique opportunities for prophylaxis, diagnosis, and therapy, as demonstrated by the success of HBV and HPV vaccines and HCV antivirals in decreasing the incidence of tumors that are caused by these viruses. Here we review common characteristics and mechanisms of action of the human oncogenic viruses.

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“…HIF‐1α overexpression has been associated with tumor cell growth and survival in head and neck tumors. Moreover, HPV is responsible for the rising proportion of OSCC and might induce the expression of oncogenes 27. Numerous expression and functional analyses have demonstrated that Notch1 plays a crucial role in the development and progression of OSCC 26.…”

Section: Discussionmentioning

confidence: 99%

Deubiquitination and stabilization of programmed cell death ligand 1 by ubiquitin‐specific peptidase 9, X‐linked in oral squamous cell carcinoma

Guo

et al. 2018

Cancer Medicine

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BackgroundThe immune checkpoint protein programmed cell death ligand 1 (PD‐L1) binds to PD1 to promote tumor cell escape from the killing effect of the immune system. However, there are few studies on the regulatory mechanisms of PD‐L1 in tumors. Although PD‐L1 has been reported to undergo ubiquitination in some cancers, its regulatory mechanisms in oral squamous cell carcinoma (OSCC) are unclear. Therefore, we aimed to investigate this phenomenon.MethodsWe examined the expression and function of USP9X and PD‐L1 in human oral keratinocytes (HOK) and OSCC cell lines (HN4 and HN30) as the control and relevant cancer cells using western blotting, immunoprecipitation, immunohistochemistry (IHC), T‐cell‐mediated tumor cell killing assay, and liquid chromatography‐mass spectrometry.ResultsProgrammed cell death ligand 1 was highly expressed in OSCC by the regulation of the ubiquitin‐proteasome pathway. Furthermore, we discovered that ubiquitin‐specific peptidase 9, X‐linked (USP9X) could be combined with PD‐L1 to induce its deubiquitination and stabilize its protein expression in OSCC.ConclusionOur data indicate that USP9X deubiquitinates and stabilizes PD‐L1. Suppressing the expression of USP9X blocks tumor cell growth. The results provide a theoretical basis for USP9X as a therapeutic target.

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Human papillomavirus molecular biology

Cited by 180 publications

References 130 publications

Oral manifestations of human papillomavirus infections

Oral manifestations of human papillomavirus infections

More than just oncogenes: mechanisms of tumorigenesis by human viruses

Deubiquitination and stabilization of programmed cell death ligand 1 by ubiquitin‐specific peptidase 9, X‐linked in oral squamous cell carcinoma

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