Up-regulated expression of Sp1 protein coincident with a viral protein in human and mouse differentiating keratinocytes may act as a cell differentiation marker

Li, Bo; Wang, Xiao; Zhou, Fang; Saunders, Nicholas A.; Frazer, Ian H.; Zhao, Kong‐Nan

doi:10.1111/j.1432-0436.2008.00300.x

Cited by 10 publications

(5 citation statements)

References 75 publications

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“…These experiments demonstrate that the PV L1 proteins, whether they were expressed by authentic or codon‐modified L1 genes, are post‐transcriptionally regulated, whereas the L1 proteins expressed from authentic or codon‐modified L1 genes in keratinocytes are differentially associated with the cell differentiation in vitro . In keeping with the in vitro findings, delivery of authentic or codon‐modified L1 genes to mouse skin using DNA particle bombardment confirms that that L1 protein was expressed from the authentic L1 genes only in the most superficial epithelial cells (Figure ), including differentiated keratinocytes in deeper hair follicles , coincident with SP1 and involucrin expression . In contrast, the codon‐modified L1 genes were expressed more extensively throughout the basal epidermis and dermis, except for the differentiated keratinocyte layers .…”

Section: Codon Usage and Viral Gene Expression In Hpvssupporting

confidence: 77%

Codon usage roles in human papillomavirus

Zhao

Chen

2011

Reviews in Medical Virology

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Human papillomavirus (HPV) genomes, similar to other virus genomes, frequently have a G + C content significantly different from their host species. The HPV genomes show a strong codon usage bias to 18 codons, with 14 showing T at the third position amongst degenerately encoded amino acids. The codon usage pattern in HPV genome plays an important role, which regulates low or non-translational expression of the viral capsid genes and results in very weak protein expression of oncogenes in a wide range of mammalian cells. Codon modification has been proved to be a powerful technology to overcome the translational blockage and weak expression of both HPV capsid genes and oncogenes in different expression systems. Furthermore, keratinocytes are the host cells of HPV infection; the codon usage in HPV capsid genes matches available aminoacyl-tRNAs in differentiated keratinocytes to modulate their protein expression. HPV DNA vaccines with codon optimization have been shown to have higher immunogenicity and induce both strong cellular and humoral responses in animal models, which may be a promising form of therapeutic HPV vaccines.

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Section: Codon Usage and Viral Gene Expression In Hpvssupporting

confidence: 77%

Codon usage roles in human papillomavirus

Zhao

Chen

2011

Reviews in Medical Virology

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“…Thus, we suggest that the up-regulation of Sp1 during the early stage of dysplasia may provoke expression of the HPV oncogenic proteins E6 and E7, and may therefore serve as a prognostic factor for cancer development. additionally, recent studies on Sp1 expression upon hpV infection showed concurrent expression of SP1 with L1 proteins in differentiating keratinocytes in mice (35).…”

Section: Discussionmentioning

confidence: 86%

IGF1 mRNA isoform expression in the cervix of HPV-positive women with pre-cancerous and cancer lesions

Koczorowska

Kwaśniewska

Goździcka-Józefiak

2010

Experimental and Therapeutic Medicine

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Abstract. human papillomavirus (hpV) plays a crucial role in cervical cancer etiology. however, not all hpV-infected women develop cancer, indicating that additional cellular factors facilitate carcinogenesis. the aim of this study was to analyze the expression profile of insulin-like growth factor 1 (iGF1) isoforms in the context of FOx2, Sp1 and iGF1 receptor (iGF1r) expression during hpV-dependent cervical carcinogenesis. One hundred and nine epithelial tissue samples from women with pre-cancerous and cancer lesions of the cervix were analyzed. HPV DNA was identified by pcr, and real-time pcr was used to quantify the expression levels of the analyzed genes. all IGF1 mrna splicing isoforms were up-regulated in pre-cancerous cells, and a shift in the balance towards mitogenic iGF1Eb was observed in the cancer samples. IGF1 expression was controlled mainly by the p1 promoter, and an increase in p2 usage was observed in the cancer. correlations between IGF1 mrna splicing isoforms and the FOx2 splicing factor, as well as p1/p2 activity and Sp1 transcription factor expression levels were detected. no correlation was observed between the expression of iGF1 and its receptor iGF1r. Our results suggest that iGF1, in particular its splicing profile, may be an additional prognostic factor in cervical carcinogenesis.

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“…Thus, mimics of severe combined immunodeficiency, WHIMS syndrome , epidermodysplasia verruciformis and related disorders in humans, are now being examined in mice using the MmuPV model, in order to establish the extent to which defects in the epithelial cell and the host immune background influence PV life cycle success versus the development of PV latency or neoplasia. In addition to the above studies, animal models have also been widely used during the development of prophylactic vaccines, and are playing an important role in the development of immunotherapeutics, although the precise nature of the model varies depending on whether the desired aim is the resolution of benign papillomas or the clearance of established cancer . Interestingly, studies on prophylactic vaccines have led to the use of a mouse model specifically to assess the efficiency of PV infection, and the ability of vaccination to protect against infection, rather than infection and disease formation.…”

Section: Control Of Papillomavirus Infection and The Development Of Vmentioning

confidence: 99%

Model systems of human papillomavirus‐associated disease

Doorbar

2015

The Journal of Pathology

124

111

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Human papillomaviruses (HPVs) cause a range of serious diseases, including the vast majority of cervical cancers, most anal cancers and around half of head and neck cancers. They are also responsible for troublesome benign epithelial lesions, including genital warts and laryngeal papillomas, and in some individuals HPVs lead to recurrent respiratory papillomatosis and other difficult-to-manage diseases. As a result, there is a great need for model systems that accurately mimic papillomavirus infections in humans. This is complicated by the diverse variety of HPVs, which now number over 200 types, and the different strategies they have evolved to persist in the population. The most well-developed models involve the culture of HPV-containing keratinocytes in organotypic raft culture, an approach which appears to accurately mimic the life cycle of several of the high-risk cancer-associated HPV types. Included amongst these are HPV16 and 18, which cause the majority of cervical cancers. The low-risk HPV types persist less well in tissue-culture models, and our ability to study the productive life cycle of these viruses is more limited. Although ongoing research is likely to improve this situation, animal models of papillomavirus disease can provide considerable basic information as to how lesions form, regress and can be controlled by the immune system. The best studied are cottontail rabbit papillomavirus, rabbit oral papillomavirus and, more recently, mouse papillomavirus (MmuPV), the last of which is providing exciting new insights into viral tropisms and immune control. In addition, transgenic models of disease have helped us to understand the consequences of persistent viral gene expression and the importance of co-factors such as hormones and UV irradiation in the development of neoplasia and cancer. It is hoped that such disease models will eventually lead us to better understanding and better treatments for human disease.

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Up-regulated expression of Sp1 protein coincident with a viral protein in human and mouse differentiating keratinocytes may act as a cell differentiation marker

Cited by 10 publications

References 75 publications

Codon usage roles in human papillomavirus

Codon usage roles in human papillomavirus

IGF1 mRNA isoform expression in the cervix of HPV-positive women with pre-cancerous and cancer lesions

Model systems of human papillomavirus‐associated disease

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