Transcriptional Regulation of Human Papillomavirus Type 18 P105 Promoter by the Co-Activator CBP

Valencia-Hernández, Armando; Cuevas, Christian; Garrido, Efraín

doi:10.1159/000112917

Cited by 8 publications

(5 citation statements)

References 77 publications

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“…CBP/p300 can also bind to the HPV18 URR in the absence of E2 as recruitment has been demonstrated in E2-negative cervical cancer cells [43]. CBP/ p300-dependent E6/E7 transcription activation is associated with acetylation of H3 at the HPV URR providing evidence that CBP/p300 activates HPV transcription by altering the epigenetic status of the viral enhancer/promoter [44]. Increased histone acetylation by CBP/p300 results in enhanced recruitment of the SWI/SNF chromatin remodelling complex catalytic subunit, the Brahma-related gene-1 (Brg1), to the URR which is required for efficient RNA polymerase II recruitment [45].…”

Section: Histone Acetylationmentioning

confidence: 81%

Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle

2020

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Human papillomaviruses (HPV) are a large family of viruses which contain a circular, double-stranded DNA genome of approximately 8000 base pairs. The viral DNA is chromatinized by the recruitment of cellular histones which are subject to host cell-mediated post-translational epigenetic modification recognized as an important mechanism of virus transcription regulation. The HPV life cycle is dependent on the terminal differentiation of the target cell within epithelia-the keratinocyte. The virus life cycle begins in the undifferentiated basal compartment of epithelia where the viral chromatin is maintained in an epigenetically repressed state, stabilized by distal chromatin interactions between the viral enhancer and early gene region. Migration of the infected keratinocyte towards the surface of the epithelium induces cellular differentiation which disrupts chromatin looping and stimulates epigenetic remodelling of the viral chromatin. These epigenetic changes result in enhanced virus transcription and activation of the virus late promoter facilitating transcription of the viral capsid proteins. In this review article, we discuss the complexity of virus-and host-cell-mediated epigenetic regulation of virus transcription with a specific focus on differentiationdependent remodelling of viral chromatin during the HPV life cycle.

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Section: Histone Acetylationmentioning

confidence: 81%

Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle

2020

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“…The CBP/p300 chromatin modulator is further recruited by the HPV18 enhanceosome to stimulate the promoter activity [92]. The activation of the HPV18 P105 promoter by the coactivator CBP directly correlates with the induction of the nucleosomal histone H3 (K14) acetylation on the HPV18 Early Promoter by CBP [93]. Brm is a chromatin remodeling protein associated with SWI/SNF complexes, which are ATP-dependent chromatin remodeling enzymes.…”

Section: Cellular Factors Involved In Viral Chromatin Remodelingmentioning

confidence: 99%

Papillomavirus interaction with cellular chromatin

You

2010

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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High-risk human papillomavirus (HPV) infection is the primary risk factor for cervical cancer. HPVs establish persistent infection by maintaining their genomes as extrachromosomal elements (episomes) that replicate along with host DNA in infected cells. The productive life cycle of HPV is intimately tied to the differentiation program of host squamous epithelium. This review examines the involvement of host chromatin in multiple aspects of the papillomavirus life cycle and the malignant progression of infected host cells. Papillomavirus utilizes host mitotic chromosomes as vehicles for transmitting its genetic materials across the cell cycle. By hitchhiking on host mitotic chromosomes, the virus ensures accurate segregation of the replicated viral episomes to the daughter cells during host cell division. This strategy allows persistent maintenance of the viral episome in the infected cells. In the meantime, the virus subverts the host chromatin-remodeling factors to promote viral transcription and efficient propagation of viral genomes. By associating with the host chromatin, papillomavirus redirects the normal cellular control of chromatin to create a cellular environment conducive to both its own survival and malignant progression of host cells. Comprehensive understanding of HPV-host chromatin interaction will offer new insights into the HPV life cycle as well as chromatin regulation. This virus-host interaction will also provide a paradigm for investigating other episomal DNA tumor viruses that share a similar mechanism for interacting with host chromatin. Papillomavirus and cancerPapillomaviruses (PVs) are small DNA tumor viruses that induce a variety of benign and malignant epithelial lesions in the infected hosts [1]. Over 140 HPV types have been identified to date. Depending on the potential for inducing malignant transformation, these viruses are further classified into high-risk and low-risk HPVs. High-risk HPVs are strongly associated with the development of cervical cancer [2], which is the second most common cancer among women worldwide and the leading cause of death from cancer among women in developing countries; approximately 500,000 cases and 275,000 deaths are reported annually. Over 97% of cervical cancers contain a high-risk HPV genome and express the viral oncogenes E6 and E7, providing a direct link between HPV infection and carcinogenesis. Currently available HPV vaccines protect against up to four major types of cancer causing strains. Alternative approaches are needed for curing ongoing infections because HPV can establish latent infections that persist for years or even decades in host cells. The deregulated expression of high-risk HPV oncogenes is a critical event for the oncogenic progression of HPV-positive lesions. In addition, substantial cytogenetic changes are needed for high-risk HPV-infected cells to progress to invasive tumors. These cellular events do not occur until many years after *Correspondence to: Jianxin You, Department of Microbiology, University of Pennsylvan...

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“…Bernat et al demonstrated using GST pull-down assays that high-risk HPV16 E7, and to a lesser extent, low-risk HPV11 E7 directly interact with p300 in vitro [47]. Using co-immunoprecipitation and mammalian two-hybrid assays, these authors also showed that HPV16 E7 interacts with p300 in vivo [48]. Additionally, they found that HPV16 E7's interaction with p300 is necessary to inhibit p300's ability to co-activate E2-driven transcription [47].…”

Section: Histone Acetylationmentioning

confidence: 99%

“…Additionally, they found that HPV16 E7's interaction with p300 is necessary to inhibit p300's ability to co-activate E2-driven transcription [47]. CBP mediates H3K14 acetylation and upregulates the transcriptional activity of the HPV18 URR [48]. HPV16 E7 associates with histone deacetylases HDAC1 and HDAC2 indirectly through Mi2β, a member of the nucleosome remodeling and histone deacetylation (NURD) complex [49,50], and this association is independent of Rb binding [50].…”

Section: Histone Acetylationmentioning

confidence: 99%

Epigenetic Regulation of the Human Papillomavirus Life Cycle

Mac

Moody

2020

Pathogens

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Persistent infection with certain types of human papillomaviruses (HPVs), termed high risk, presents a public health burden due to their association with multiple human cancers, including cervical cancer and an increasing number of head and neck cancers. Despite the development of prophylactic vaccines, the incidence of HPV-associated cancers remains high. In addition, no vaccine has yet been licensed for therapeutic use against pre-existing HPV infections and HPV-associated diseases. Although persistent HPV infection is the major risk factor for cancer development, additional genetic and epigenetic alterations are required for progression to the malignant phenotype. Unlike genetic mutations, the reversibility of epigenetic modifications makes epigenetic regulators ideal therapeutic targets for cancer therapy. This review article will highlight the recent advances in the understanding of epigenetic modifications associated with HPV infections, with a particular focus on the role of these epigenetic changes during different stages of the HPV life cycle that are closely associated with activation of DNA damage response pathways.

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Transcriptional Regulation of Human Papillomavirus Type 18 P105 Promoter by the Co-Activator CBP

Cited by 8 publications

References 77 publications

Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle

Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle

Papillomavirus interaction with cellular chromatin

Epigenetic Regulation of the Human Papillomavirus Life Cycle

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