scholarly journals The Role of HPV E6 and E7 Oncoproteins in HPV-associated Cervical Carcinogenesis

2005 ◽  
Vol 37 (6) ◽  
pp. 319 ◽  
Author(s):  
Eun-Kyoung Yim ◽  
Jong-Sup Park
Keyword(s):  
Cervical Carcinogenesis ◽  
Hpv E6 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

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.

scholarly journals Association of cervical carcinogenesis risk with HPV16 E6 and E7 variants in the Taizhou area, China

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mei-Zhen Dai ◽  
Yi Qiu ◽  
Xing-Hong Di ◽  
Wei-Wu Shi ◽  
Hui-Hui Xu
Keyword(s):  
Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Chi Square ◽  
Major Health Problem ◽  
Hpv16 E6 ◽  
Exact Test ◽  
Chi Square Test ◽  
E6 And E7

Abstract Background Human papillomavirus (HPV) type 16 accounts for a larger share of cervical cancer and has been a major health problem worldwide for decades. The progression of initial infection to cervical cancer has been linked to viral sequence properties; however, the role of HPV16 variants in the risk of cervical carcinogenesis, especially with longitudinal follow-up, is not fully understood in China. Methods We aimed to investigate the genetic variability of HPV16 E6 and E7 oncogenes in isolates from cervical exfoliated cells. Between December 2012 and December 2014, a total of 310 single HPV16-positive samples were selected from women living in the Taizhou area, China. Sequences of all E6 and E7 oncogenes were analysed by PCR-sequencing assay. Detailed sequence comparison, genetic heterogeneity analyses and maximum-likelihood phylogenetic tree construction were performed with BioEdit Sequence Alignment Editor and MEGA X software. Data for cytology tests and histological diagnoses were obtained from our Taizhou Area Study with longitudinal follow-up for at least 5 years. The relationship between HPV16 variants and cervical carcinogenesis risk was analysed by the chi-square test or Fisher’s exact test. Results In this study, we obtained 64 distinct variation patterns with the accession GenBank numbers MT681266-MT681329. Phylogenetic analysis revealed that 98.3% of HPV16 variants belong to lineage A, in which the A4 (Asian) sublineage was dominant (64.8%), followed by A2 (12.1%), A1 (11.4%), and A3 (10.0%). The A4 (Asian) sublineage had a higher risk of CIN2+ than the A1–3 (European) sublineages (OR = 2.69, 95% CI = 1.04–6.97, P < 0.05). Furthermore, nucleotide variation in HPV16 E6 T178G is associated with the development of cervical cancer. Conclusion These data could provide novel insights into the role of HPV16 variants in cervical carcinogenesis risk in China.

scholarly journals Upregulation of PIR gene expression induced by human papillomavirus E6 and E7 in epithelial oral and cervical cells

Open Biology ◽  
2017 ◽  
Vol 7 (11) ◽  
pp. 170111 ◽  
Author(s):  
Diego Carrillo ◽  
Juan P. Muñoz ◽  
Hernán Huerta ◽  
Gabriel Leal ◽  
Alejandro Corvalán ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Papillomavirus ◽  
Dna Microarrays ◽  
Epithelial Mesenchymal Transition ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Hpv E6 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7 ◽  
Oral Cells

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.

scholarly journals High levels of p105 (NFKB1) and p100 (NFKB2) proteins in HPV16-transformed keratinocytes: role of E6 and E7 oncoproteins

Virology ◽  
2005 ◽  
Vol 331 (2) ◽  
pp. 357-366 ◽  
Author(s):  
L. Havard ◽  
S. Rahmouni ◽  
J. Boniver ◽  
P. Delvenne
Keyword(s):  
E6 And E7 Oncoproteins ◽  
E6 And E7

Role of E6 and E7 oncoproteins in HPV-induced anogenital malignancies

1996 ◽  
Vol 7 (5) ◽  
pp. 295-304 ◽  
Author(s):  
Michael H.G. Kubbutat ◽  
Karen H. Vousden
Keyword(s):  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals The Role of the Human Papillomavirus (HPV) in Cervical Cancer: A Review about HPV-Induced Carcinogenesis and Its Epidemiology, Diagnosis, Management and Prevention

2016 ◽  
Vol 4 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Karl Bonello ◽  
Renald Blundell
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cervical Neoplasia ◽  
Diagnostic Tools ◽  
Cervical Carcinogenesis ◽  
Epidemiological Factors ◽  
Micro Rnas ◽  
E6 And E7

The human papillomavirus (HPV) was the first virus known to induce carcinogenesis and is associated with cancers of the uterine cervix, anogenital tumors and malignancies of the head and neck. This paper reviews the structure and basic genomic characteristics of the virus and outlines the clinical involvement of the main HPV serotypes, focusing on the carcinogenic role of HPV-16 and 18. The mechanisms that occur in the development of cervical neoplasia due to the oncogenic proteins E6 and E7 which interfere with the regulation of the cell cycle through their interaction with p53 and retinoblastoma protein are described. Epidemiological factors, diagnostic tools and the management of the disease are also reviewed, along with the available vaccines to prevent the viral infection. Insights on current research on involvement of oxidative stress and micro-RNAs in cervical carcinogenesis are also explored as they may unlock new means of diagnosis and treatment in the future.

Sign in / Sign up

Export Citation Format

Share Document