Relevant bibliographies by topics / E7 oncoprotein

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Academic literature on the topic 'E7 oncoprotein'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "E7 oncoprotein"

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DeMasi, Joseph, Michael C. Chao, Ashu S. Kumar, and Peter M. Howley. "Bovine Papillomavirus E7 Oncoprotein Inhibits Anoikis." Journal of Virology 81, no. 17 (June 27, 2007): 9419–25. http://dx.doi.org/10.1128/jvi.00422-07.

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ABSTRACT The bovine papillomavirus type 1 (BPV-1) E7 oncoprotein is required for the full transformation activity of the virus. Although BPV-1 E7 by itself is not sufficient to induce cellular transformation, it enhances the abilities of the other BPV-1 oncogenes to induce anchorage independence. We have been exploring the mechanisms by which E7 might affect the transformation efficiency of other viral oncoproteins and in particular whether it might protect cells from apoptosis. We report here that BPV-1 E6 and E7 can each independently inhibit anoikis, a type of apoptosis that is induced upon cell detachment. Using site-directed mutagenesis, we determined regions of the E7 protein that were essential for its antiapoptotic activity. The ability of E7 to inhibit anoikis did partially correlate with an ability to enhance anchorage independence of BPV-1 E6-transformed cells. In addition, the antiapoptotic activity of E7 also only partially correlated with its ability to bind p600, a cellular protein that has previously been reported to play a role in anoikis. We conclude that the contribution of E7 to BPV-induced cellular transformation may involve its ability to inhibit anoikis but that additional functional activities must also be involved.
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Zhang, Jin-Jun, Xin-Chun Cao, Xiang-Yu Zheng, Hai-Ying Wang, and Yong-Wei Li. "Feasibility study of a human papillomavirus E6 and E7 oncoprotein test for the diagnosis of cervical precancer and cancer." Journal of International Medical Research 46, no. 3 (January 11, 2018): 1033–42. http://dx.doi.org/10.1177/0300060517736913.

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Objective To evaluate the clinical value of human papillomavirus (HPV) E6 and E7 oncoprotein (HPV E6/E7) detection in the early screening of cervical cancer. Methods This prospective study evaluated all patients with suspected cervical intraepithelial neoplasia (CIN) as identified by the presence of at least one positive indicator from a ThinPrep cytologic test (TCT) and/or a Hybrid Capture 2 (HC2) HPV DNA test. The levels of E6/E7 oncoproteins were determined using Western blot analysis. The diagnostic value of the HPV E6/E7 protein assay was compared with the clinical diagnosis from TCT, HC2 and the gold standard of cervical biopsy histology. Results A total of 450 patients were enrolled in the study and based on histological findings, 102 patients were diagnosed with CIN1 (22.7%), 241 with CIN2 (53.6%), 96 with CIN3 (21.3%) and 11 with squamous cell carcinoma (2.4%). For a diagnosis of CIN2+, although the sensitivity of the HPV E6/E7 assay was lower than HC2 (65.5% versus 96.6%, respectively), the specificity was higher (38.2% versus 5.9%, respectively). The sensitivity of the HPV E6/E7 assay was higher than TCT (65.5% versus 36.2%, respectively). Conclusion Measuring HPV E6/E7 oncoprotein levels is a potential new biomarker for HPV type 16.
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McLaughlin-Drubin, Margaret E., and Karl Münger. "The human papillomavirus E7 oncoprotein." Virology 384, no. 2 (February 2009): 335–44. http://dx.doi.org/10.1016/j.virol.2008.10.006.

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Tang, Shuang, Mingfang Tao, J. Philip McCoy, and Zhi-Ming Zheng. "The E7 Oncoprotein Is Translated from Spliced E6*I Transcripts in High-Risk Human Papillomavirus Type 16- or Type 18-Positive Cervical Cancer Cell Lines via Translation Reinitiation." Journal of Virology 80, no. 9 (May 1, 2006): 4249–63. http://dx.doi.org/10.1128/jvi.80.9.4249-4263.2006.

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ABSTRACT High-risk human papillomaviruses (HPVs) encode two viral oncoproteins, E6 and E7, from a single bicistronic pre-mRNA containing three exons and two introns. Retention of intron 1 in the E6 coding region is essential for production of the full-length E6 oncoprotein. However, splicing of intron 1 is extremely efficient in cervical cancer cells, leading to the production of a spliced transcript, E6*I, of E6. Here, we investigated whether this splicing of intron 1 might benefit E7 production. Using RNA interference as a tool, we targeted the intron 1 region using small interfering RNAs (siRNAs) in HPV-positive cell lines. At an effective low dose, the siRNAs specifically suppressed E6 expression but not E7 expression, as demonstrated by the stabilization of p53. However, at high doses the HPV18 intron 1-specific siRNA substantially and specifically reduced the level of the 18E6*I mRNA lacking the intron region in HeLa cells, implying its nuclear silencing on the pre-mRNA before RNA splicing. Two other siRNAs targeting the exon 2 regions of HPV16 and -18, which encode the E7 oncoprotein, reduced the E6*I mRNAs to a remarkable extent and preferentially suppressed expression of E7, leading to accumulation of hypophosphorylated p105Rb and cell cycle arrest, indicating that the majority of E7 proteins are the translational products of E6*I mRNAs. This was confirmed by transient transfection in 293 cells: E7 could be translated only from the E7 open reading frame (ORF) on E6*I mRNA in a distance-dependent matter of upstream E6*I ORF by translation reinitiation. The data thus provide direct evidence that the E6*I mRNAs of high-risk HPVs are responsible for E7 production.
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Carrillo, Diego, Juan P. Muñoz, Hernán Huerta, Gabriel Leal, Alejandro Corvalán, Oscar León, Gloria M. Calaf, et al. "Upregulation of PIR gene expression induced by human papillomavirus E6 and E7 in epithelial oral and cervical cells." Open Biology 7, no. 11 (November 2017): 170111. http://dx.doi.org/10.1098/rsob.170111.

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The hallmark of high-risk human papillomavirus (HR-HPV)-related carcinogenesis is E6 and E7 oncogene overexpression. The aim of this work was to characterize epithelial oral and cervical cancer cells that express HR-HPV E6 and E7 oncoproteins. Transcriptomic assay using DNA microarrays revealed that PIR gene expression was detected in oral cells in an HR-HPV E6/E7-dependent manner. In addition, PIR was overexpressed in HPV-positive SiHa and Ca Ski cells, whereas it was undetectable in HPV-negative C33A cells. The PIR expression was dependent on functional HR-HPV E6 and E7 oncoproteins even though the E7 oncoprotein had higher activity to induce PIR overexpression in comparison with E6. In addition, using an siRNA for PIR silencing in oral cells ectopically expressing HR-HPV E6/E7, there was a significant increase in E-cadherin transcripts and a decrease in Vimentin, Slug, Zeb and Snail transcripts, suggesting that HR-HPV-induced PIR overexpression is involved in epithelial–mesenchymal transition. Furthermore, migration of PIR-silenced cells was significantly decreased. Finally, using inhibitors of some specific pathways, it was found that EGFR/ERK and PI3 K/AKT signalling pathways are important for E7-mediated PIR overexpression. It can be concluded that PIR gene expression is highly dependent on the expression of HR-HPV oncoproteins and is important for EMT regulation.
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Carrillo-Beltrán, Diego, Juan P. Muñoz, Nahir Guerrero-Vásquez, Rancés Blanco, Oscar León, Vanesca de Souza Lino, Julio C. Tapia, et al. "Human Papillomavirus 16 E7 Promotes EGFR/PI3K/AKT1/NRF2 Signaling Pathway Contributing to PIR/NF-κB Activation in Oral Cancer Cells." Cancers 12, no. 7 (July 15, 2020): 1904. http://dx.doi.org/10.3390/cancers12071904.

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A subset of oral carcinomas is etiologically related to high-risk human papillomavirus (HR-HPV) infection, with HPV16 being the most frequent HR-HPV type found in these carcinomas. The oncogenic role of HR-HPV is strongly dependent on the overexpression of E6 and E7 oncoproteins, which, in turn, induce p53 and pRb degradation, respectively. Additionally, it has been suggested that HR-HPV oncoproteins are involved in the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), inducing cancer progression and metastasis. Previously, we reported that HPV16 E7 oncoprotein promotes Pirin upregulation resulting in increased epithelial–mesenchymal transition (EMT) and cell migration, with Pirin being an oxidative stress sensor and activator of NF-κB. In this study, we demonstrate the mechanism by which HPV16 E7-mediated Pirin overexpression occurs by promoting EGFR/PI3K/AKT1/NRF2 signaling, thus causing PIR/NF-κB activation in oral tumor cells. Our results demonstrate a new mechanism by which E7 contributes to oral cancer progression, proposing PIR as a potential new therapeutic target.
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Taghizadeh, Eskandar, Sepideh Jahangiri, Daryoush Rostami, Forough Taheri, Pedram Ghorbani Renani, Hassan Taghizadeh, and Seyed Mohammad Gheibi Hayat. "Roles of E6 and E7 Human Papillomavirus Proteins in Molecular Pathogenesis of Cervical Cancer." Current Protein & Peptide Science 20, no. 9 (September 17, 2019): 926–34. http://dx.doi.org/10.2174/1389203720666190618101441.

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Human papillomavirus (HPV) cancers are expected to be major global health concerns in the upcoming decades. The growth of HPV-positive cancer cells depends on the consistent expression of oncoprotein which has been poorly taken into account in the cellular communication. Among them, E6/E7 oncoproteins are attractive therapeutic targets as their inhibition rapidly leads to the onset of aging in HPV-positive cancer cells. This cellular response is associated with the regeneration of p53, pRb anti-proliferative proteins as well as the mTOR signaling pathway; hence, the identification of involved and application of E6/E7 inhibitors can lead to new therapeutic strategies. In the present review, we focused on the pathogenicity of E6/E7 Proteins of human papillomavirus and their roles associated with the cervical cancer.
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Hu, Renjian, Zhen Dong, Kui Zhang, Guangzhao Pan, Chongyang Li, and Hongjuan Cui. "Preparation, Characterization and Diagnostic Valuation of Two Novel Anti-HPV16 E7 Oncoprotein Monoclonal Antibodies." Viruses 12, no. 3 (March 19, 2020): 333. http://dx.doi.org/10.3390/v12030333.

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At present, the clinical detection method of human papillomavirus (HPV) is mainly based on the PCR method. However, this method can only be used to detect HPV DNA and HPV types, and cannot be used to accurately predict cervical cancer. HPV16 E7 is an oncoprotein selectively expressed in cervical cancers. In this study, we prepared an HPV16 E7-histidine (HIS) fusion oncoprotein by using a prokaryotic expression and gained several mouse anti-HPV16 E7-HIS fusion oncoprotein monoclonal antibodies (mAbs) by using hybridoma technology. Two mAbs, 69E2 (IgG2a) and 79A11 (IgM), were identified. Immunocytochemistry, immunofluorescence, immunohistochemistry, and Western blot were used to characterize the specificity of these mAbs. The sequences of the nucleotide bases and predicted amino acids of the 69E2 and 79A11 antibodies showed that they were novel antibodies. Indirect enzyme-linked immunosorbent assay (ELISA) with overlapping peptides, indirect competitive ELISA, and 3D structural modeling showed that mAbs 69E2 and 79A11 specifically bound to the three exposed peptides of the HPV16 E7 (HPV16 E749–66, HPV16 E773–85, and HPV16 E791–97). We used these two antibodies (79A11 as a capture antibody and 69E2 as a detection antibody) to establish a double-antibody sandwich ELISA based on a horseradish peroxidase (HRP)-labeled mAb and tetramethylbenzidine (TMB) detection system for quantitative detection of the HPV16 E7-HIS fusion oncoprotein, however, it was not ideal. Then we established a chemiluminescence immunoassay based on a labeled streptavidin-biotin (LSAB)-ELISA method and luminol detection system—this was sufficient for quantitative detection of the HPV16 E7-HIS fusion oncogenic protein in ng levels and was suitable for the detection of HPV16-positive cervical carcinoma tissues. Collectively, we obtained two novel mouse anti-HPV16 E7 oncoprotein mAbs and established an LSAB-lumino-dual-antibody sandwich ELISA method for the detection of the HPV16 E7-HIS fusion oncogenic protein, which might be a promising method for the diagnosis of HPV16-type cervical cancers in the early stage.
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McFarlane, Melanie, Alasdair I. MacDonald, Andrew Stevenson, and Sheila V. Graham. "Human Papillomavirus 16 Oncoprotein Expression Is Controlled by the Cellular Splicing Factor SRSF2 (SC35)." Journal of Virology 89, no. 10 (February 25, 2015): 5276–87. http://dx.doi.org/10.1128/jvi.03434-14.

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ABSTRACTHigh-risk human papillomaviruses (HR-HPV) cause anogenital cancers, including cervical cancer, and head and neck cancers. Human papillomavirus 16 (HPV16) is the most prevalent HR-HPV. HPV oncogenesis is driven by two viral oncoproteins, E6 and E7, which are expressed through alternative splicing of a polycistronic RNA to yield four major splice isoforms (E6 full length, E6*I, E6*II, E6*X). The production of multiple mRNA isoforms from a single gene is controlled by serine/arginine-rich splicing factors (SRSFs), and HPV16 infection induces overexpression of a subset of these, SRSFs 1, 2, and 3. In this study, we examined whether these proteins could control HPV16 oncoprotein expression. Small interfering RNA (siRNA) depletion experiments revealed that SRSF1 did not affect oncoprotein RNA levels. While SRSF3 knockdown caused some reduction in E6E7 expression, depletion of SRSF2 resulted in a significant loss of E6E7 RNAs, resulting in reduced levels of the E6-regulated p53 proteins and E7 oncoprotein itself. SRSF2 contributed to the tumor phenotype of HPV16-positive cervical cancer cells, as its depletion resulted in decreased cell proliferation, reduced colony formation, and increased apoptosis. SRSF2 did not affect transcription from the P97promoter that controls viral oncoprotein expression. Rather, RNA decay experiments showed that SRSF2 is required to maintain stability of E6E7 mRNAs. These data show that SRSF2 is a key regulator of HPV16 oncoprotein expression and cervical tumor maintenance.IMPORTANCEExpression of the HPV16 oncoproteins E7 and E6 drives HPV-associated tumor formation. Although increased transcription may yield increased levels of E6E7 mRNAs, it is known that the RNAs can have increased stability upon integration into the host genome. SR splicing factors (SRSFs) control splicing but can also control other events in the RNA life cycle, including RNA stability. Previously, we demonstrated increased levels of SRSFs 1, 2, and 3 during cervical tumor progression. Now we show that SRSF2 is required for expression of E6E7 mRNAs in cervical tumor but not nontumor cells and may act by inhibiting their decay. SRSF2 depletion in W12 tumor cells resulted in increased apoptosis, decreased proliferation, and decreased colony formation, suggesting that SRSF2 has oncogenic functions in cervical tumor progression. SRSF function can be targeted by known drugs that inhibit SRSF phosphorylation, suggesting a possible new avenue in abrogating HPV oncoprotein activity.
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Bello-Rios, Ciresthel, Sarita Montaño, Olga Lilia Garibay-Cerdenares, Lilian Esmeralda Araujo-Arcos, Marco Antonio Leyva-Vázquez, and Berenice Illades-Aguiar. "Modeling and Molecular Dynamics of the 3D Structure of the HPV16 E7 Protein and Its Variants." International Journal of Molecular Sciences 22, no. 3 (January 30, 2021): 1400. http://dx.doi.org/10.3390/ijms22031400.

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The oncogenic potential of high-risk human papillomavirus (HPV) is predicated on the production of the E6 and E7 oncoproteins, which are responsible for disrupting the control of the cell cycle. Epidemiological studies have proposed that the presence of the N29S and H51N variants of the HPV16 E7 protein is significantly associated with cervical cancer. It has been suggested that changes in the amino acid sequence of E7 variants may affect the oncoprotein 3D structure; however, this remains uncertain. An analysis of the structural differences of the HPV16 E7 protein and its variants (N29S and H51N) was performed through homology modeling and structural refinement by molecular dynamics simulation. We propose, for the first time, a 3D structure of the E7 reference protein and two of Its variants (N29S and H51N), and conclude that the mutations induced by the variants in N29S and H51N have a significant influence on the 3D structure of the E7 protein of HPV16, which could be related to the oncogenic capacity of this protein.
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Dissertations / Theses on the topic "E7 oncoprotein"

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AMARAL, Carolina Maria Medeiros Do. "Avaliação da presença do Papilomavírus humano (HPV) em tumores de pulmão." Universidade Federal de Pernambuco, 2015. https://repositorio.ufpe.br/handle/123456789/18464.

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FACEPE
Os Papilomavírus humano (HPV) infectam mucosas e epitélio contribuindo para o desenvolvimento de tumores benignos como também malignos. São amplamente conhecidos como causadores do câncer cervical, contudo, atualmente, vem apresentando evidências de associação com diversos outros tipos de canceres, como o câncer de pulmão. Sendo assim, o presente estudo avaliou a presença do DNA do HPV em tumores de pulmão de pacientes do Estado de Pernambuco bem como a expressão de suas oncoproteínas E6 e E7. Para isto, a detecção foi feita em amostras de tecidos de tumores frescos e parafinados de 63 pacientes. HPV estava presente em 52% das amostras, sendo detectados os tipos 16 e 18 com frequências de 81 e 19%, respectivamente. Quanto a presença do vírus nos diferentes tipos histológicos dos tumores, foi detectado HPV em 40% dos carcinomas escamosos, 33% dos adenocarcinomas, 18% dos carcinomas de células pequenas e 9% em carcinoma de células grandes. Através da técnica de imunohistoquimica detectou-se a presença das oncoproteinas virais E6 (anticorpo anti-HPV 16 e anti-HPV 18) e E7 (anticorpo anti-HPV 16 e anti-HPV 18) com frequências de 85 e 75%, respectivamente. Tal resultado confirma os resultados obtidos molecularmente quanto à presença do HPV e é sugestivo de que o vírus esteja em atividade nas células tumorais e provavelmente esteja desempenhando um papel na carcinogênese de pulmão. No entanto, mais estudos são necessários para se ter um maior esclarecimento sobre interação de E6 e E7 com proteínas celulares na tumorigenese pulmonar.
Small DNA viruses - Human Papillomavirus (HPV) - infect oral mucosa and the epthelium, which leads to the development of both benign and malign tumors. They are widely known as the principal causes of cervical cancer although currently there is evidence to show that they are associated with several other types of cancer, such as lung cancer. In the light of this, this study evaluated the presence of HPV in the tumors of lungs of patients from the State of Pernambuco, as well as the E6 and E7 oncoproteins expression. This involved carrying out the detection in tumor tissue samples that were fresh and paraffin-embedded and taken from 63 patients. HPV was found to be present in 52% of the samples, and types 16 and 18 were detected with frequencies of 81% and 19% respectively. With regard to the presence of the vírus in different histological types of tumors, HPV was detected in 40% of the squamous carcinomas, 33% of the adenocarcinomas, 18% of the small cell carcinomas and 9% in large cell carcinomas. The presence of the E6 (antibody anti-HPV 16 and anti-HPV 18) and E7 (antibody anti-HPV 16 and anti-HPV 18) oncoproteins was detected by means of the immunohistochemical technique and this confirmed the results obtained from a molecular analysis with regard to the presence of the virus and it is suggestive that the virus is active in tumor cells and is probably playing a role in lung carcinogenesis. However, further studies are required to have a clearer understanding of the interaction of E6 and E7 with the cell proteins in pulmonary tumorigenesis.
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Onder, Zeynep. "Characterization of the Nucleocytoplasmic Transport of the Cutaneous HPV8 E7 Protein." Thesis, Boston College, 2014. http://hdl.handle.net/2345/3828.

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Thesis advisor: Junona Moroianu
Some non melanoma skin cancers (NMSC) have been associated with human papillomavirus (HPV) pathogenesis, like epidermodysplasia verruciformis (EV) and squamous cell carcinoma (SCC). EV is a genetically inherited skin disease that develops when the individuals are infected with cutaneous HPV types belonging to the β-genus, especially types 5 and 8. Transgenic mouse lineages expressing all early genes of cutaneous HPV8 develop papillomas, dysplasias and SCC after UV irradiation and this correlates with enhanced HPV8 oncogenes expression. We have previously discovered that the nuclear localization of mucosal HPV16 E7 and HPV11 E7 proteins is mediated by their zinc-binding domain via a Ran-dependent pathway and independent of nuclear import receptors and that a patch of hydrophobic residues within the zinc-binding domain of HPV16 E7 and HPV11 E7 proteins is responsible for their nuclear import via hydrophobic interactions with FG nucleoporins. Here we investigated the nucleocytoplasmic traffic of cutaneous HPV8 E7 protein using confocal microscopy to analyze the intracellular localization of EGFP-8E7, its subdomains and its mutants after transient transfections. We also investigated the nuclear import ability of GST-8E7, its subdomains and mutants using in vitro nuclear import assays in digitonin-permeabilized HeLa cells. In addition, we performed isolation assays to study the direct interaction between HPV8 E7 and two FG nucleoporins, Nup62 and Nup153 or the nuclear export receptor, CRM1. We found that the nuclear import of cutaneous HPV8 E7 is mediated by a nuclear localization signal (NLS) located within its zinc-binding domain. Furthermore, we determined that the hydrophobic residues within the 65LRLFV69 patch are responsible for the nuclear import and nuclear localization of HPV8 E7 via direct hydrophobic interactions with FG nucleoporins, Nup62 and Nup153, whereas the positively charged arginine 66 plays no significant role in the function of the NLS. In addition, we examined the nuclear export mechanism of cutaneous HPV8 E7 protein and showed that it has a leucine-rich nuclear export signal (NES) in its C-terminal domain that is recognized by the CRM1 nuclear export receptor. These studies are essential for understanding the nucleocytoplasmic traffic of cutaneous HPV8 E7 protein
Thesis (PhD) — Boston College, 2014
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Eberhard, Jeremy. "Studies on the Nucleocytoplasmic Transport of the E7 Oncoprotein of High-Risk HPV Type 16." Thesis, Boston College, 2013. http://hdl.handle.net/2345/3293.

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Thesis advisor: Junona Moroianu
Human papillomaviruses (HPVs) have been estimated to be the most common sexually transmitted infection in the United States. In addition to condyloma accuminata, infection of the squamous basal epithelium by high-risk HPVs, notably type 16 (HPV16), has been shown to be the primary etiological agent in the majority of cervical carcinomas. The E7 major transforming protein of HPV16, along with E6, has been linked to tumorigenesis and malignancy. While the E7 protein itself possesses no enzymatic activity, its ability to bind a number of nuclear and cytoplasmic targets subverts a variety of cellular regulatory complexes and facilitates viral replication. Previous studies in the Moroianu Lab have shown the HPV16 E7 oncoprotein to translocate across the nuclear pore complex (NPC) in a facilitated manner dependent on a non-canonical, c-terminal, nuclear localization signal (cNLS) for import, and a consensus leucine-rich nuclear export sequence (NES) for export (28). While the leucine-rich NES has been characterized, a full examination of the cNLS has yet to be performed. Here we present evidence that the karyopherin independent nuclear import mediated by the cNLS of 16E7 is dependent on its c-terminal Zn binding domain. Furthermore, we demonstrate that nuclear import is mediated by the direct interaction of a small patch of hydrophobic residues, 65LRLCV69, with the FG domain of the central FG-nucleoporin Nup62. In addition, we examined a potential regulatory mechanism of 16E7 nucleocytoplasmic translocation. Previous work has shown that a serine conserved in the high-risk HPVs at position 71 is phosphorylated by an unknown kinase. Here we present evidence that while phosphorylation of S71 is not required for either 16E7 nuclear localization or nuclear export in HeLa cells, mimicking phosphorylation of the S71 residue results in a statistically significant shift in the distribution of localization phenotypes of the resultant cell population toward a larger percentage exhibiting more nuclear localization. These data suggest that nucleocytoplasmic transport of 16E7 is, at least in part, a regulated process
Thesis (PhD) — Boston College, 2013
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Nicol, Clare. "Selection and characterisation of RNA aptamers to the human papillomavirus 16 (HPV16) E7 oncoprotein." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535664.

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Yu, Yueyang. "Induction of Mitotic Alterations by the Human Papillomavirus Type 16 E7 Oncoprotein: Mechanistic Studies." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11112.

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High-risk human papillomaviruses (HPVs) are causative agents of most cervical cancers and a significant portion of other anogenital tract and oral carcinomas. The major oncogenic activities of HPV16 E6 and E7 oncoproteins are associated with the degradation of the p53 and retinoblastoma tumor suppressors, respectively. E6 also causes increased expression of the catalytic subunit of telomerase, hTERT. In addition, E6 and E7 contribute to carcinogenesis through induction of genomic instability. Accurate chromosome segregation during mitosis is essential for preservation of genomic stability and HPV16 E7 perturbs mitosis in several ways. HPV16 E7 induces the synthesis of supernumerary centrosomes and increases the incidence of multipolar mitoses, which can lead to chromosome missegregation. Moreover, HPV16 E7 expression causes a prometaphase delay, which usually reflects an activation of the mitotic spindle assembly checkpoint (SAC), yet some studies suggested that the SAC is abrogated in HPV16 E7-expressing cells.
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Eichten, Alexandra. "Functional interactions between the human papillomavirus type 16 E7 oncoprotein and the tumor suppressor p53." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96635429X.

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Helt, Anna-Marija. "Multiple biological activities of the human papillomavirus type 16 E7 oncoprotein contribute to the abrogation of human epithelial cell cycle control /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/11514.

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LIMA, Elyda Gonçalves de. "Detecção e análise do Papilomavírus humano (HPV) em carcinomas mamários de mulheres do Nordeste do Brasil." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/19530.

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O câncer da mama é o tipo de câncer que mais acomete mulheres em todo o mundo. Diversos fatores estãoassociados ao desenvolvimento desta neoplasia, dentre elas as infecções virais. Entre os três vírus mais estudados como causa de carcinogênese mamária está oPapillomavirus humano (HPV). Assim, oobjetivo foi detectar e analisar o HPV emcarcinomasmamáriosde mulheres do Nordeste do Brasil. A detecção do DNA viral foi realizada PCR, as amostras positivasforam tipificadas por sequenciamento. A quantificação da carga viral e a determinação do status físico por qPCR, e a detecção as oncoproteínas de E6 e E7 de HPV por imunohistoquímica. O DNA de HPV foi detectado em 46,7% dos carcinomas de mama HPV-positivos. O HPV16foi omais prevalente, 92% dos casos. A carga viral do HPV apresentou uma média de 14,2 cópias em 104 células, noscarcinomas de mama. Além disso, em 57,2% dos carcinomas mamáriosHPV-positivas apresentaram o DNA viral integrado ao genoma do hospedeiro. Altas taxas de detecção das oncoproteínas E6(89,5%) e E7(90%) foram identificadas nos carcinomas de mama HPV-positivos. Já as proteínas supressoras de tumor, p53 e p16INK4A, apresentaram taxas menores 95,7% e 92,3% respectivamente. Os resultados deste estudo sugerem que o vírus esteja em atividade nas células tumorais e provavelmente desempenhem papel na carcinogênese mamária.
Breast cancer is the type of cancer that affects more women around the world. Several factors are associated with the development of cancer, among which viral infections. Of the three most-studied virus as a cause of mammary carcinogenesis is the Human papillomavirus (HPV). The objective was to detect and analyze HPV in breast carcinomas of women in northeastern Brazil. The detection of viral DNA was performed PCR positive samples were typed by sequencing. The quantification of viral load and to determine the physical status by qPCR, and detection of the oncoproteins E6 and HPV E7 by immunohistochemistry. HPV DNA was detected in 46.7% of HPV-positive breast carcinomas. HPV16 was the most prevalent, 92% of cases. The HPV viral load averaged 14.2 copies in 104 cells in breast carcinomas. Furthermore, 57.2% of HPV-positive breast carcinomas showed the integrated viral DNA into the host genome. High rates of detection of E6 (89.5%) and E7 (90%) were identified in HPV-positive breast tumors. Already the tumor suppressor protein p53 and p16INK4a, had lower rates 95.7% and 92.3% respectively. The results of this study suggests that the virus is active in tumor cells and probably play role in breast carcinogenesis.
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Ricciardi, Riccardo Pietro 1985. "A role for high-risk HPV type 16 E6 and E7 oncoproteins in colorecteral carcinogenesis /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112351.

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Human papillomavirus (HPV) infections play a crucial role in human carcinogenesis. Greater than 96% of all cervical carcinomas are positive for high-risk HPV infections; especially types 16 and 18. High-risk HPV onco-proteins, E6 and E7, are consistently expressed in such cancers and function by inactivating p53 and pRb tumor suppressors, respectively. The presence of high-risk HPVs is also correlated with anogenital cancers. In this study, we examined the effect of high-risk HPV type 16 E6 and E7 oncoproteins in two normal human colorectal epithelial cell lines, NCE1 and NCE5. We report that the expression of E6/E7 proteins, alone, induced cellular transformation of both cell lines; consequently, NCE1-E6/E7 and NCE5-E6/E7 form colonies in soft agar with respect to their wild type cells. This is accompanied by cell cycle deregulation, as is demonstrated by the over-expression of cyclin dependant kinases (cdks) and their respective cyclins. Furthermore, we demonstrate that E6/E7 oncoprotein transduction induces migration of colorectal epithelial cells. More still, well analyzed Id gene expression, a family member of the helix-loop-helix (HLH) transcription factors involved in the regulation of cell invasion and metastasis of human cancer cells. In parallel, using tissue microarray analysis we found that the four members of the Id protein family are correlated with the presence of HPV type 16 and 18 in human colon cancer tissues. Our data suggests that high-risk HPV infections are sufficient to induce cellular transformation of normal human colorectal cells, in vitro. Furthermore, the correlation with the Id family of proteins may present a novel set of markers associated with HPV induced colorectal carcinogenesis. Our results may suggest a new approach to detect and prevent colorectal cancer.
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Pacini, Laura. "Deregulation of TLR9 signalling pathway in human keratinocytes by E6 and E7 oncoproteins from beta human papillomavirus type 38." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1321/document.

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Les virus du papillome humain (HPV) sont des virus à ADN double-brin encapsidés appartenant à la famille des Papillomaviridae ayant un tropisme distinct pour les épithéliums squameux de type muqueux ou cutanés. Jusqu'à présent, plus de 200 types de HPV ont été isolés et regroupés dans un arbre phylogénétique composé de 5 genres nommés alpha, beta, gamma, mu et nu. Parmi eux, les types HPV muqueux à haut risque appartenant au genre alpha ont été associés au cancer du col de l'utérus ainsi qu'à des sous-groupes de carcinomes ano-génitaux et de la tête et du cou. Ces virus sont responsables d'environ 5% de tous les cancers viro-induits. Les types bêta du HPV ont un tropisme pour la peau et pourraient être impliqués dans le développement du cancer de la peau non mélanique (NMSC), en association avec la lumière ultraviolette (UV). Ainsi, les modèles expérimentaux in vitro et in vivo ont démontré les propriétés de transformation des oncoprotéines E6 et E7 du type HPV bêta 38. De plus, des études sur le modèle de souris transgénique, où E6 et E7 du HPV38 sont exprimés au niveau de la couche basale non différenciée de l'épithélium sous le contrôle du promoteur du gène humain de la kératine (K14), ont montré une très forte susceptibilité de la peau à la carcinogenèse induite par les UV par rapport aux animaux de type sauvage. Tout aussi important que leur capacité à promouvoir la transformation cellulaire, les virus oncogènes ont développé différentes stratégies pour prendre le dessus sur le système immunitaire de l'hôte, favorisant ainsi l'établissement d'une infection persistante. Par conséquent, savoir si des virus oncogènes potentiels ont la capacité d'interférer avec la réponse immunitaire pourrait fournir des preuves supplémentaires de leur implication dans la cancérogenèse humaine. Ici, nous montrons que les oncoprotéines E6 et E7 de HPV38 suppriment l'expression de Tolllike 9 (TLR9), récepteur des ADN double-brins, en favorisant l'accumulation de ΔNp73α, un antagoniste de p53 et p73. Des expériences d'immunoprécipitation de la chromatine ont montré que ΔNp73α fait partie d'un complexe de régulation négative transcriptionnelle qui se lie à un élément de réponse NF-kappaB dans le promoteur TLR9. Fait intéressant, l'expression ectopique de TLR9 dans des cellules HPV38 E6E7 a entraîné une accumulation des inhibiteurs du cycle cellulaire p21WAF1/Cip1 et p27kip1, une réduction de l'activité kinase associée à CDK2 et l'inhibition de la prolifération cellulaire. Ensemble, ces données indiquent que TLR9 est impliqué dans d'autres événements, en plus de la réponse immunitaire innée. Par conséquent, nous avons constaté que le traitement des kératinocytes humains primaires (HPK) avec différents stress cellulaires, par exemple l'irradiation aux UV, la doxorubicine et le traitement H2O2, conduisent à une induction de la transcription de TLR9. Cet évènement induit par les UV est arbitré par le recrutement de plusieurs facteurs de transcription sur le promoteur TLR9, tels que p53, NF-kappaB p65 et c-Jun. L'expression de E6 et E7 de HPV38 affecte fortement le recrutement de ces facteurs de transcription sur le promoteur TLR9, avec comme conséquence l'affaiblissement de l'expression du gène TLR9. En résumé, nos données montrent que HPV38, de manière similaire à d'autres virus avec une activité oncogénique bien connue, peut inhiber 'expression de TLR9. Plus important encore, nous mettons en évidence une nouvelle fonction de TLR9 dans le contrôle de la réponse cellulaire aux stress et nous montrons que E6 et E7 de HPV38 sont capables d'interférer avec un tel mécanisme. Ces résultats confirment le rôle des types HPV bêta dans la carcinogenèse de la peau, en fournissant des informations supplémentaires sur leur contribution précise dans le processus multi-étapes de développement du cancer
The human papillomaviruses (HPV) consist of a group of capsid-enclosed double-stranded deoxyribonucleic acid (dsDNA) viruses from the Papillomaviridae family that display a distinct tropism for mucosal or cutaneous squamous epithelia. Until now, more than 200 types of HPV have been isolated and grouped into a phylogenetic tree composed of 5 genera (alpha, beta, gamma, mu and nu papillomaviruses). Among them, the mucosal high-risk HPV types that belong to the genus alpha have been associated with cervical cancer as well as a subset of anogenital and head and neck carcinomas. They are responsible for approximately 5% of all virus-induced cancers. Beta HPV types have a skin tropism and have been suggested to be involved, together with ultraviolet light (UV), in the development of non-melanoma skin cancer (NMSC). For instance, in vitro and in vivo experimental models highlight the transforming properties of beta HPV38 E6 and E7. Specifically, studies of transgenic mouse model, where HPV38 E6 and E7 are expressed in the undifferentiated basal layer of epithelia under the control of the Keratin 14 (K14) promoter, showed a very high susceptibility to UV-induced skin carcinogenesis in comparison to the wild-type animals. Equally important as their ability to promote cellular transformation, oncogenic viruses have different strategies to overtake the host immune system thus guaranteeing persistent infection. Therefore, understanding whether potential oncogenic viruses have the ability to interfere with the immune response could provide additional evidence relating to their involvement in human carcinogenesis. Here, we show that the E6 and E7 oncoproteins from HPV38 suppress the expression of the dsDNA innate immune sensor Toll-like receptor 9 (TLR9) by promoting the accumulation of ΔNp73α, an antagonist of p53 and p73. Chromatin immunoprecipitation experiments showed that ΔNp73α is part of a negative transcriptional regulatory complex that binds to a NF-κB responsive element within the TLR9 promoter. Interestingly, ectopic expression of TLR9 in HPV38 E6E7 cells resulted in an accumulation of the cell cycle inhibitors p21WAF/Cip1 and p27Kip1, reduction of CDK2-associated kinase activity and inhibition of cellular proliferation. Together these data indicate that TLR9 is involved in additional events, besides the innate immune response. Accordingly, we observed that the treatment of human primary keratinocytes (HPKs) with different cellular stresses, e.g. UV irradiation, doxorubicin and H2O2 treatment, results in TLR9 up-regulation. This UVinduced event is mediated by the recruitment of several transcription factors to the TLR9 promoter, such as p53, NF-kB p65 and c-Jun. The expression of HPV38 E6 and E7 strongly affect the recruitment of these transcription factors to the TLR9 promoter, with consequent impairment of TLR9 gene expression. In summary, our data show that HPV38, similarly to other viruses with well-known oncogenic activity, can down-regulate TLR9. Most importantly, we highlight a novel function of TLR9 in controlling the cellular response to stresses and we show that HPV38 E6 and E7 are able to interfere with such mechanism. These findings further support the role of beta HPV types in skin carcinogenesis, providing additional insight into their precise contribution to the multistep process of cancer development
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Books on the topic "E7 oncoprotein"

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Tommasino, Massimo. Papillomaviruses in Human Cancer: The Role Of E6 And E7 Oncoproteins. Springer, 2013.

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1958-, Tommasino Massimo, ed. Papillomaviruses in human cancer: The role of E6 and E7 oncoproteins. New York: Springer, 1997.

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Tommasino, Massimo. Papillomaviruses in Human Cancer: The Role of E6 and E7 Oncoproteins (Molecular Biology Intelligence Unit). Landes Bioscience, 1997.

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Papillomaviruses in Human Cancer: The Role of E6 and E7 Oncoproteins (Molecular Biology Intelligence Unit Series). Springer, 1999.

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Book chapters on the topic "E7 oncoprotein"

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Chardonnet, Y., A. Janiaud, J. J. Chomel, J. Viac, S. Euvrard, D. Schmitt, and M. Aymard. "Detection by Elisa Test of Antibodies to Human Papillomavirus (HPV) Type 16 E7 Oncoprotein in Patients with Benign or Malignant Papillomas from Skin or Mucosa." In Immunology of Human Papillomaviruses, 133–38. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_23.

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Korzeniewski, Nina, and Stefan Duensing. "Disruption of Centrosome Duplication Control and Induction of Mitotic Instability by the High-Risk Human Papillomavirus Oncoproteins E6 and E7." In The Centrosome, 201–21. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-035-9_12.

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Zwerschke, Werner, and Pidder Jansen-Dürr. "Cell Transformation by the E7 Oncoprotein of Human Papillomavirus Type 16: Interactions with Nuclear and Cytoplasmic Target Proteins." In Advances in Cancer Research, 1–29. Elsevier, 1999. http://dx.doi.org/10.1016/s0065-230x(08)61022-2.

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Tommasino, Massimo. "Molecular Mechanisms of E6 and E7 Oncoproteins From Human Papillomaviruses in Cellular Transformation." In DNA Tumour Viruses: Virology, Pathogenesis and Vaccines. Caister Academic Press, 2018. http://dx.doi.org/10.21775/9781910190791.03.

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McBride, Alison A., Elliot J. Androphy, and Karl Münger. "Regulation of the Papillomavirus E6 and E7 Oncoproteins By the Viral E1 and E2 Proteins." In Viral Regulatory Structures and their Degeneracy, 35–52. CRC Press, 2018. http://dx.doi.org/10.1201/9780429503238-2.

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Widyaputra, Sunardhi, Natallia Pranata, Ignatius Setiawan, and Jamas Ari Anggraini. "The Presence of HPV in Dental Calculus: It’s Role in Pathogenesis of Oral and Cervical Cancer." In Cervical Cancer - A Global Public Health Treatise [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98347.

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Human papillomavirus (HPV) infection accounts for approximately 5.2% of the worldwide human cancer burden. Molecular epidemiologic evidence clearly indicates that certain types of HPV are the principal cause of both cervical and oral cancers. Major oncoproteins E6 and E7 can inactivate p53 and pRB proteins because it happened genome instability and dysregulation host cell cycles. This virus is an epithelial tropism, vulnerable area mainly at the basal layer and epithelial stem cell, because it still has a high proliferation capacity, so it can support the replication of the virus. Virions bind initially to the glycosaminoglycan (GAG) chains of heparan sulphate proteoglycan (HSPG). More than 99% cervical cancer arise at the cervical transformation zone. In oral cavity, exposed areas of the basal layer will be very susceptible to HPV infection. The HPV presence in the oral area is considered as one of the etiologics of oral cancer in those who do not have bad habits such as smoking, betel chewing, or poor oral hygiene. Our study successfully identified HPV type 58 in dental calculus. Dental calculus, calcified oral plaque biofilm, has been shown to be an abundant, nearly ubiquitous, and long-term reservoir of the ancient oral microbiome, including bacteria, archaea, eukaryote, and viruses. During biomineral maturation process, several biological contents around the oral region should be trapped, including the exfoliated virus contained cells. Dental calculus is a promising source of HPV and carcinogens molecules in the oral cavity and could be used as a biomarker for early detection.
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Conference papers on the topic "E7 oncoprotein"

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Korzeniewski, Nina, Anette Duensing, and Stefan Duensing. "Abstract 5354: HPV-16 E7 oncoprotein induces centriole multiplication through deregulation of PLK4, a master regulator of centriole biogenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5354.

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Leung, SOA, S. Feldman, and K. Elias. "188 Point-of-care surrogate biomarkers for cervical cancer screening: feasibility of E7 oncoprotein and P16INK4A detection in cervical samples." In IGCS Annual 2019 Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-igcs.188.

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Jing, K., S. Shin, and K. Lim. "PO-123 Constitutive expression of FAT1 gene inhibits the invasion and tumorigenicity of cervical cancer cells through degradation of HPV E6/E7 oncoprotein via P53/RBin vitroandin vivo." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.164.

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Toussaint-Smith, Esra, and Ann Roman. "The Role of Human Papillomavirus 16 E6 and E7 Oncoproteins in Angiogenesis." In Minority Trainee Research Forum, 2004. TheScientificWorld Ltd, 2004. http://dx.doi.org/10.1100/tsw.2004.152.

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McGhee, Eva, Lucy Tran, Mengtao Li, Yong Wu, Seyung Chung, Cheryl Araniego, Karen Tate, et al. "Abstract 4588: Estrogen receptor alpha mediates HPV E6/E7 oncoproteins: Induced breast cells proliferation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4588.

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McGhee, Eva, Mengtao Li, Yi-Ling Lin, Liliana Zarate, Naomi Long, Mai Do, Chinelo Ezechukwu, et al. "Abstract 3326: Upregulation of epigenetic changes acquired by HPV16 E6/E7 oncoproteins in mouse keratinocytes: Targeting ATM/PI3K." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3326.

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McGhee, Eva, Liliana Zarate, Chiamaka Opara, Antoinette Alugbue, Meidrah Tyler, Bileko Wissa, Billy Ballard, and Roland Pattillo. "Abstract 5342: Epigenetic polymorphisms and human papillomavirus E6/E7 oncoproteins transfection: Induce ATM gene deletion11q22-23 and chromosomal instability." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5342.

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Tate, Karen, Lucy Tran, Melanie Baker, Kamilah Evans, Mechelle Rouse, Seyung Chung, Duy Nguyen, et al. "Abstract 4072: Molecular cytogenetic characterization of HPV types 16 and 18 cervical cancers: Acquired genomic instability by E6 and E7 oncoproteins." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4072.

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Do, Mai, Nichelle Cox, Naomi Long, Liliana Zarate, Chinelo Ezechukwu, Jenna Cormier, Hyun Chung, et al. "Abstract 3388: Molecular characterization of HPV type 18 cervical cancer: Upregulation of telomerase expression and induced chromosomal instability by E6 and E7 oncoproteins." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3388.

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Hochmann Valls, JP, F. Parietti, J. Martinez, AC Lopez, M. Carreño, C. Quijano, L. Sichero, M. Möller, S. Mirazo, and J. Arbiza. "117 Cooperative effect of human papillomavirus type 18 e5, e6 e7 oncoproteins in promoting cell proliferation, migration, invasion and in modulating cellular redox state." In IGCS Annual 2019 Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-igcs.117.

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