scholarly journals Modulation of DNA methylation by human papillomavirus E6 and E7 oncoproteins in cervical cancer (Review)

2017 ◽  
Author(s):  
Prakriti Sen ◽  
Pooja Ganguly ◽  
Niladri Ganguly
Keyword(s):  
Cervical Cancer ◽  
Dna Methylation ◽  
Human Papillomavirus ◽  
Cancer Review ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

Antibodies against linear and conformational epitopes of the human papillomavirus (HPV) type 16 E6 and E7 oncoproteins in sera of cervical cancer patients

1994 ◽  
Vol 137 (3-4) ◽  
pp. 341-353 ◽  
Author(s):  
I. Nindl ◽  
L. Benitez-Bribiesca ◽  
J. Berumen ◽  
N. Farmanara ◽  
S. Fisher ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Patients ◽  
Conformational Epitopes ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals Monoclonal Antibodies Against Human Papillomavirus E6 and E7 Oncoproteins Inhibit Tumor Growth in Experimental Cervical Cancer

2019 ◽  
Vol 12 (10) ◽  
pp. 1289-1295 ◽  
Author(s):  
Zewei Jiang ◽  
Joseph Albanese ◽  
Joshua Kesterson ◽  
Joshua Warrick ◽  
Rouzan Karabakhtsian ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Monoclonal Antibodies ◽  
Human Papillomavirus ◽  
Tumor Growth ◽  
Inhibit Tumor Growth ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals The Efficacy of Therapeutic DNA Vaccines Expressing the Human Papillomavirus E6 and E7 Oncoproteins for Treatment of Cervical Cancer: Systematic Review

Vaccines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 53
Author(s):  
Ayazhan Akhatova ◽  
Chee Kai Chan ◽  
Azliyati Azizan ◽  
Gulzhanat Aimagambetova
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Public Health Problem ◽  
Clinical Implementation ◽  
Therapeutic Vaccines ◽  
Term Survival ◽  
Hpv E6 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7 ◽  
Lesion Regression

Cervical cancer is recognized as a serious public health problem since it remains one of the most common cancers with a high mortality rate among women despite existing preventative, screening, and treatment approaches. Since Human Papillomavirus (HPV) was recognized as the causative agent, the preventative HPV vaccines have made great progress over the last few years. However, people already infected with the virus require an effective treatment that would ensure long-term survival and a cure. Currently, clinical trials investigating HPV therapeutic vaccines show a promising vaccine-induced T-cell mediated immune response, resulting in cervical lesion regression and viral eradication. Among existing vaccine types (live vector, protein-based, nucleic acid-based, etc.), deoxyribonucleic acid (DNA) therapeutic vaccines are the focus of the study, since they are safe, cost-efficient, thermostable, easily produced in high purity and distributed. The aim of this study is to assess and compare existing DNA therapeutic vaccines in phase I and II trials, expressing HPV E6 and E7 oncoproteins for the prospective treatment of cervical cancer based on clinical efficacy, immunogenicity, viral clearance, and side effects. Five different DNA therapeutic vaccines (GX-188E, VGX-3100, pNGVL4a-CRT/E7(detox), pNGVL4a-Sig/E7(detox)/HSP70, MEDI0457) were well-tolerated and clinically effective. Clinical implementation of DNA therapeutic vaccines into treatment regimen as a sole approach or in combination with conservative treatment holds great potential for effective cancer treatment.

E6 and E7 oncoproteins: Potential targets of cervical cancer

2020 ◽  
Vol 27 ◽  
Author(s):  
Ramarao Malla ◽  
Mohammad Amjad Kamal
Keyword(s):  
Cervical Cancer ◽  
Drug Resistance ◽  
Host Cell ◽  
Molecular Mechanisms ◽  
Immune Therapy ◽  
Cervical Lesions ◽  
Diagnostic Strategies ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

: Cervical cancer (CC) is the fourth leading cancer in women in the age group 15-44 globally. Experimental as well as epidemiological studies identified that type16 and 18 HPV cause 70% of precancerous cervical lesions as well as cervical cancer worldwide by bringing about genetic as well as epigenetic changes in the host genome. The insertion of the HPV genome triggers various defense mechanisms including the silencing of tumor suppressor genes as well as activation of oncogenes associated with cancer metastatic pathway. E6 and E7 are small oncoproteins consisting of 150 and 100 amino acids respectively. These oncoproteins affect the regulation of the host cell cycle by interfering with p53 and pRb. Further these oncoproteins adversely affect the normal functions of the host cell by binding to their signaling proteins. Recent studies demonstrated that E6 and E7 oncoproteins are potential targets for CC. Therefore, this review discusses the role of E6 and E7 oncoproteins in metastasis and drug resistance as well as their regulation, early oncogene mediated signaling pathways. This review also uncovers the recent updates on molecular mechanisms of E6 and E7 mediated phytotherapy, gene therapy, immune therapy, and vaccine strategies as well as diagnosis through precision testing. Therefore, understanding the potential role of E6/E7 in metastasis and drug resistance along with targeted treatment, vaccine, and precision diagnostic strategies could be useful for the prevention and treatment of cervical cancer.

E6 and E7 Oncoproteins from Human Papillomavirus Type 16 Induce Activation of Human Transforming Growth Factorβ1Promoter throughout Sp1 Recognition Sequence

2006 ◽  
Vol 19 (3) ◽  
pp. 468-480 ◽  
Author(s):  
Oscar Peralta-Zaragoza ◽  
Víctor Bermúdez-Morales ◽  
Lourdes Gutiérrez-Xicotencatl ◽  
Juan Alcocer-González ◽  
Félix Recillas-Targa ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Recognition Sequence ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals Multiple ASF/SF2 Sites in the Human Papillomavirus Type 16 (HPV-16) E4-Coding Region Promote Splicing to the Most Commonly Used 3′-Splice Site on the HPV-16 Genome

2010 ◽  
Vol 84 (16) ◽  
pp. 8219-8230 ◽  
Author(s):  
Monika Somberg ◽  
Stefan Schwartz
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Splice Site ◽  
Binding Sites ◽  
Mrna Levels ◽  
Coding Region ◽  
Cervical Lesions ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7

ABSTRACT Our results presented here demonstrate that the most abundant human papillomavirus type 16 (HPV-16) mRNAs expressing the viral oncogenes E6 and E7 are regulated by cellular ASF/SF2, itself defined as a proto-oncogene and overexpressed in cervical cancer cells. We show that the most frequently used 3′-splice site on the HPV-16 genome, site SA3358, which is used to produce primarily E4, E6, and E7 mRNAs, is regulated by ASF/SF2. Splice site SA3358 is immediately followed by 15 potential binding sites for the splicing factor ASF/SF2. Recombinant ASF/SF2 binds to the cluster of ASF/SF2 sites. Mutational inactivation of all 15 sites abolished splicing to SA3358 and redirected splicing to the downstream-located, late 3′-splice site SA5639. Overexpression of a mutant ASF/SF2 protein that lacks the RS domain, also totally inhibited the usage of SA3358 and redirected splicing to the late 3′-splice site SA5639. The 15 ASF/SF2 binding sites could be replaced by an ASF/SF2-dependent, HIV-1-derived splicing enhancer named GAR. This enhancer was also inhibited by the mutant ASF/SF2 protein that lacks the RS domain. Finally, silencer RNA (siRNA)-mediated knockdown of ASF/SF2 caused a reduction in spliced HPV-16 mRNA levels. Taken together, our results demonstrate that the major HPV-16 3′-splice site SA3358 is dependent on ASF/SF2. SA3358 is used by the most abundantly expressed HPV-16 mRNAs, including those encoding E6 and E7. High levels of ASF/SF2 may therefore be a requirement for progression to cervical cancer. This is supported by our earlier findings that ASF/SF2 is overexpressed in high-grade cervical lesions and cervical cancer.

scholarly journals Human papilloma virus, DNA methylation and microRNA expression in cervical cancer (Review)

2014 ◽  
Vol 31 (6) ◽  
pp. 2467-2476 ◽  
Author(s):  
HILDA JIMÉNEZ-WENCES ◽  
OSCAR PERALTA-ZARAGOZA ◽  
GLORIA FERNÁNDEZ-TILAPA
Keyword(s):  
Cervical Cancer ◽  
Dna Methylation ◽  
Human Papilloma Virus ◽  
Microrna Expression ◽  
Papilloma Virus ◽  
Cancer Review
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