scholarly journals Involvement of the Toll-Like Receptor/Nitric Oxide Signaling Pathway in the Pathogenesis of Cervical Cancer Caused by High-Risk Human Papillomavirus Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Jie Li ◽  
Heping Rao ◽  
Chang’e Jin ◽  
Jinrong Liu
Keyword(s):  
Nitric Oxide ◽  
Cervical Cancer ◽  
Human Papillomavirus ◽  
High Risk ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Cervical Canal ◽  
Toll Like Receptor ◽  
No Signaling ◽  
Cervical Epithelial Cells

Human papillomavirus (HPV) can activate Toll-like receptor (TLR)/nitric oxide (NO) signaling pathways; however, whether the TLR/NO pathway is involved in cervical cancer caused by high-risk HPV (HR-HPV) remains unclear. In this study, 43 HR-HPV-positive patients with cervical cancer (CC group), 39 HR-HPV-positive patients with a healthy cervix (HR-HPV group), and 33 HR-HPV-negative controls were recruited. NO concentration in cervical canal and expression of inducible NO synthase (iNOS) in cervical tissues were detected. Expressions of key TLR/NO pathway genes (TLR3/4/7/8, NF-κB p65, and iNOS) in cervical epithelial cells were detected by quantitative reverse transcription PCR. Expressions of TLR4, NF-κB p65, and iNOS in CaSki, HeLa, and C33a cells were determined by Western blot. NO concentration in cervical canal of CC group was significantly higher than in other groups (P<0.05). Positive rates of iNOS in cervical tissues were 72.1%, 28.2%, and 3.1% in the CC group, HR-HPV group, and controls, respectively (P<0.05). Levels of TLR3, TLR4, TLR7, TLR8, NF-κB p65, and iNOS in cervical epithelial cells were higher in CC group than in other groups (P<0.05). Both mRNA and protein levels of TLR4, NF-κB p65, and iNOS were higher in HPV-positive HeLa and CaSki cells than in HPV-negative C33a cells (P<0.05). Together, these results suggest that TLR/NO signaling pathway may be involved in pathogenesis of cervical cancer caused by HR-HPV.

scholarly journals Plasma-based Endogenous Metabolomics Profiling of High-Risk Human Papillomavirus and Their Emerging Roles in the Progression of Cervical Cancer

2021 ◽  
Author(s):  
Qin Wang ◽  
Min Xu ◽  
Tingting Chen ◽  
Jing Chen ◽  
Runjie Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
High Risk ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Metabolic Phenotype ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: High-risk human papillomavirus (HR-HPV) is the main etiological factor for cervical cancer. Accumulating evidence has suggested that the active role of metabolites in the initiation and progression of cancers. This study was to explore the metabolic profiles of HR-HPV infection and their potential functions in cervical cancer.Methods: Non-targeted metabolomics approach was used to detect metabolic alterations in the plasma obtained from HPV-16 positive (HPV16 (+)), HPV-18 positive (HPV18 (+)) and HPV negative (CTL) individuals, followed by CCK8 experiment to detect the effect of different metabolites on the proliferation of Hela and GH354. A cell migration test then verified significant metabolites on the migration of Hela and GH354. Q RT-qPCR and western blot were used to detect malignant progression related mRNA and protein expression levels of cervical cancer.Results: HR-HPV groups shared 24 dysregulated metabolites (such as amino acids, ceramides, glycerophosphocholines). Further experiments showed ceramide species, including C8 inhibits cervical cancer cells proliferation and migration in vitro. In contrast, C12 significantly enhanced cervical cancer cells proliferation and migration in vitro. Protein and mRNA expressions indicated C8 and C12 were related to the malignant behavior of cervical cancer in vitro. The underlying mechanism demonstrated that C8 intervention inhibited proliferation and migration in cervical cancer cells via the MAPK/JNK signaling pathway, while C12 intervention promoted proliferation and migration in cervical cancer cells via the MAPK/ERK signaling pathway. These findings may contribute to the treatment of HR-HPV-induced cervical cancer by intervening in its initiation and progression.Conclusion: Our study shed some light on how metabolites influenced the relationship between HR-HPV oncogenic capability and metabolic phenotype change and identify species C8 and C12 as critical lipid metabolites that modulate cervical cancer cell’s function.

scholarly journals Distribution and location of Daxx in cervical epithelial cells with high risk human papillomavirus positive

2014 ◽  
Vol 9 (1) ◽  
pp. 1 ◽  
Author(s):  
Shuang-yang Tang ◽  
Le Li ◽  
Yao-lin Li ◽  
An-yuan Liu ◽  
Min-jun Yu ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
High Risk ◽  
Epithelial Cells ◽  
Cervical Epithelial Cells

scholarly journals Key Molecular Events in Cervical Cancer Development

Medicina ◽  
2019 ◽  
Vol 55 (7) ◽  
pp. 384 ◽  
Author(s):  
Shandra Devi Balasubramaniam ◽  
Venugopal Balakrishnan ◽  
Chern Ein Oon ◽  
Gurjeet Kaur
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Human Papillomavirus ◽  
High Risk ◽  
Epithelial Cells ◽  
Neoplastic Progression ◽  
Cervical Lesions ◽  
Host Chromosome ◽  
Molecular Events

Cervical cancer is the fourth most common cancer among women. Infection by high-risk human papillomavirus (HPV) is the main aetiology for the development of cervical cancer. Infection by high-risk human papillomavirus (HPV) and the integration of the HPV genome into the host chromosome of cervical epithelial cells are key early events in the neoplastic progression of cervical lesions. The viral oncoproteins, mainly E6 and E7, are responsible for the initial changes in epithelial cells. The viral proteins inactivate two main tumour suppressor proteins, p53, and retinoblastoma (pRb). Inactivation of these host proteins disrupts both the DNA repair mechanisms and apoptosis, leading to rapid cell proliferation. Multiple genes involved in DNA repair, cell proliferation, growth factor activity, angiogenesis, as well as mitogenesis genes become highly expressed in cervical intraepithelial neoplasia (CIN) and cancer. This genomic instability encourages HPV-infected cells to progress towards invasive carcinoma. The key molecular events involved in cervical carcinogenesis will be discussed in this review.

scholarly journals The Human Papillomavirus Type 31 Late 3′ Untranslated Region Contains a Complex Bipartite Negative Regulatory Element

2002 ◽  
Vol 76 (12) ◽  
pp. 5993-6003 ◽  
Author(s):  
Sarah A. Cumming ◽  
Claire E. Repellin ◽  
Maria McPhillips ◽  
Jonathan C. Radford ◽  
J. Barklie Clements ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Papillomavirus ◽  
High Risk ◽  
Epithelial Cells ◽  
Regulatory Element ◽  
Capsid Proteins ◽  
Cellular Proteins ◽  
Late Gene Expression ◽  
Hpv 16 ◽  
Negative Regulatory Element

ABSTRACT The papillomavirus life cycle is tightly linked to epithelial cell differentiation. Production of virus capsid proteins is restricted to the most terminally differentiated keratinocytes in the upper layers of the epithelium. However, mRNAs encoding the capsid proteins can be detected in less-differentiated cells, suggesting that late gene expression is controlled posttranscriptionally. Short sequence elements (less than 80 nucleotides in length) that inhibit gene expression in undifferentiated epithelial cells have been identified in the late 3′ untranslated regions (UTRs) of several papillomaviruses, including the high-risk mucosal type human papillomavirus type 16 (HPV-16). Here we show that closely related high-risk mucosal type HPV-31 also contains elements that can act to repress gene expression in undifferentiated epithelial cells. However, the HPV-31 negative regulatory element is surprisingly complex, comprising a major inhibitory element of approximately 130 nucleotides upstream of the late polyadenylation site and a minor element of approximately 110 nucleotides mapping downstream. The first 60 nucleotides of the major element have 68% identity to the negative regulatory element of HPV-16, and these elements bind the same cellular proteins, CstF-64, U2AF65, and HuR. The minor inhibitory element binds some cellular proteins in common with the major inhibitory element, though it also binds certain proteins that do not bind the upstream element.

scholarly journals Thioredoxin Reductase Is Essential for Protection ofNeisseria gonorrhoeaeagainst Killing by Nitric Oxide and for Bacterial Growth during Interaction with Cervical Epithelial Cells

2009 ◽  
Vol 199 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Adam J. Potter ◽  
Stephen P. Kidd ◽  
Jennifer L. Edwards ◽  
Megan L. Falsetta ◽  
Michael A. Apicella ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Bacterial Growth ◽  
Thioredoxin Reductase ◽  
Cervical Epithelial Cells

Polymorphism of TP53 gene and the risk of high human papillomavirus load in cervical epithelial cells

Gene Reports ◽  
2022 ◽  
Vol 26 ◽  
pp. 101456
Author(s):  
Abbas Hadi Albosale ◽  
Olga Andreevna Garbuzova ◽  
Konstantin Alekseevich Kovalenko ◽  
Elena Vladimirovna Mashkina
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Cells ◽  
Tp53 Gene ◽  
Cervical Epithelial Cells

scholarly journals Prevalence and Genotyping of Human Papillomavirus (HPV) in Female with High-Risk Behaviour in Dhaka, Bangladesh

1970 ◽  
Vol 25 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Tahmina Sultana ◽  
Mohsina Huq ◽  
Anadil Alam ◽  
Dipak Kumar Mitra ◽  
Donald James Gomes
Keyword(s):  
Cervical Cancer ◽  
Polymerase Chain Reaction ◽  
Human Papillomavirus ◽  
High Risk ◽  
General Population ◽  
Sex Workers ◽  
Chain Reaction ◽  
Hpv Types ◽  
Polymerase Chain ◽  
High Risk Hpv

In developing countries, cervical cancer is the most common cause of cancer related to mortality in women. But the epidemiology of human papillomavirus (HPV) in different areas of Bangladesh is largely unknown both in risk groups and in the general population. The objective of the present study was to determine the risk factors associated with having HPV and the prevalence of high-risk HPV types among women with highrisk behaviour and to assess its potential impact on preventive strategies as the sex workers are at increased risk for sexually transmitted infections (STI), HPV and hence cervical cancer. Cervical swab from 293 sex workers in Dhaka City between August and September 2003 and between February 2005 and May 2006 were screened for HPV DNA using an HPV short fragment (E6) polymerase chain reaction (PCR) based assay. HPV positive samples were genotyped with nested multiplex polymerase chain reaction (NMPCR) for the highrisk types. The overall HPV prevalence in sex workers was 75.8%, whereas for the high risk type it was 49.8%. Prevalence of single genotype and multiple types of HPV was 33.1 and 16.7% respectively. The most prevalent high-risk HPV types, in order of prevalence rate, were HPV16, HPV18, HPV58, HPV45, HPV31 and HPV33. Both HPV 16 and HPV 18 were present in 21% of the cases. Targeting HPV 16 and 18 with prophylactic vaccines could possibly have an important impact on the incidence of invasive cervical carcinoma in this group of women. Primary prevention and cervical cancer screening programmes should be optimized more and run yearly among the general population. It is proposed to screen sex workers when they enter prostitution regardless of their age. Keywords: Human papillomavirus (HPV); High-risk HPV types; Cervical cancer; Sex workersDOI: http://dx.doi.org/10.3329/bjm.v25i1.4861 Bangladesh J Microbiol, Volume 25, Number 1, June 2008, pp 65-68

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