scholarly journals Cervical Squamous Intraepithelial Lesions Are Associated with Differences in the Vaginal Microbiota of Mexican Women

Author(s):  
M. E. Nieves-Ramírez ◽  
O. Partida-Rodríguez ◽  
P. Moran ◽  
A. Serrano-Vázquez ◽  
H. Pérez-Juárez ◽  
...  

Human papillomavirus (HPV) plays a critical role in cervical carcinogenesis but is not sufficient for cervical cancer development, indicating the involvement of other factors. The vaginal microbiota is an important factor in controlling infections caused by HPV, and, depending on its composition, it can modulate the microenvironment in vaginal mucosa against viral infections.

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Heng Zou ◽  
Huijia Chen ◽  
Shuaibin Liu ◽  
Xiaoling Gan

Abstract Background Circular RNAs (circRNAs) are increasingly implicated in regulating human carcinogenesis. Previous work showed the oncogenic activity of circ_0018289 in cervical cancer. However, the molecular basis underlying the modulation of circ_0018289 in cervical carcinogenesis is still not fully understood. Methods The levels of circ_0018289, microRNA (miR)-183-5p, and transmembrane p24 trafficking protein 5 (TMED5) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Ribonuclease (RNase) R and subcellular localization assays were used to characterize circ_0018289. Cell proliferation was detected by the Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (Edu) assays. Cell apoptosis and tube formation were assessed by flow cytometry and tube formation assays, respectively. A dual-luciferase reporter assay was performed to confirm the direct relationship between miR-183-5p and circ_0018289 or TMED5. The role of circ_0018289 in tumor growth was gauged by mouse xenograft experiments. Results Circ_0018289 was overexpressed in cervical cancer tissues and cells. Circ_0018289 silencing impeded cell proliferation, enhanced cell apoptosis, and suppressed angiogenesis in vitro, as well as diminished tumor growth in vivo. Mechanistically, circ_0018289 targeted and regulated miR-183-5p by binding to miR-183-5p, and circ_0018289 regulated cervical cancer development and angiogenesis partially through miR-183-5p. Moreover, TMED5 was directly targeted and inhibited by miR-183-5p through the perfect complementary sites in TMED5 3′UTR, and TMED5 knockdown phenocopied miR-183-5p overexpression in suppressing cervical cancer development and angiogenesis. Furthermore, circ_0018289 induced TMED5 expression by competitively binding to shared miR-183-5p. Conclusion Our observations identified the circ_0018289/miR-183-5p/TMED5 regulatory network as a novel molecular basis underlying the modulation of cervical carcinogenesis.


2020 ◽  
Vol 73 (2) ◽  
pp. 157-160
Author(s):  
María del Carmen Colín-Ferreyra ◽  
Ma. Victoria Domínguez-García ◽  
Hugo Mendieta-Zerón ◽  
María del Socorro Camarillo-Romero ◽  
Michelle Pérez-Rogel ◽  
...  

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 5594-5594
Author(s):  
A. P. Coelho ◽  
A. Nogal ◽  
D. Pereira ◽  
A. Matos ◽  
B. Sousa ◽  
...  

5594 Background: Cervical cancer (ICC) and squamous intraepitelial lesions of the cervix uteri (SIL) constitute serious health problems to women worldwide. ICC occupies the second place in the list of tumours afflicting women. Around 470,000 new cases are diagnosed annually, 80% of which in less developed countries and near half of them resulting in death of the women. MCP-1 chemokine is the main determinant of tumour associated macrophages (TAM) content in the squamous cell carcinoma of the uterine cervix. The aim of our study was the evaluation of the association between the -2518 MCP-1 polymorphism (a biallelic G/A functional polymorphism) and susceptibility to cervical intraepithelial lesions and cervical cancer development. Methods: We analyzed 898 samples of DNA, of which 420 corresponded to healthy women (control group), 130 to women with low and high-grade cervical intraepithelial lesions and 348 to women with cervical cancer. The analysis of the polymorphism and the evaluation of the corresponding genotypes were performed with the PCR-RFLP methodology. Analysis of data was performed using the computer software SPSS for windows. Results: The analysis of the genotipic frequencies of the -2518 MCP-1 genotypes indicates that women carrying genotypes with the G allele present a 29.2% protection for the development of intraepithelial lesions of the cervix uteri (OR=0.708; 95% CI: 0.503–0.998; P=0.048) and a 33.5% protection for the development of squamous cell carcinoma of the cervix uteri. It was also possible to observe an association between the waiting time to onset of cervical cancer and the polymorphism: 59 years for women carrying genotypes with the G allele (95% CI: 56–61years) and 53 years for women with the AA genotype (95% CI: 52–57 years; P=0.005). Also, women with genotypes carrying the G allele present a 2.5 fold higher risk for the progression from early stages of invasive cervical carcinoma (I/II) to clinically more advanced stages (III/IV) (OR=2.26; 95% CI: 1.09–4.67; P=0.026). Conclusions: These findings suggest a role of the -2518 MCP-1 polymorphism in the molecular mechanisms that lead to cervical cancer development and progression. No significant financial relationships to disclose.


2021 ◽  
Author(s):  
ME Nieves-Ramírez ◽  
O Partida-Rodríguez ◽  
P Moran ◽  
A Serrano-Vázquez ◽  
H Pérez-Juárez ◽  
...  

ABSTRACTCervical cancer is an important health concern worldwide and is one of the leading causes of deaths in Mexican women. Previous studies have shown changes in the female genital tract microbe community related to Human Papillomavirus (HPV) infection and cervical cancer, yet this link remains unexplored in many human populations. This study evaluated the vaginal bacterial community among Mexican women with pre-cancerous Squamous Intraepithelial Lesions (SIL). We sequenced the V3 region of the 16S rRNA gene (Illumina Miseq) in cervical samples from 300 Mexican women, including 157 patients with SIL, most of which were HPV positive, and 143 healthy women without HPV infection or SIL. Beta-diversity analysis showed that 14.6% of the variance in vaginal bacterial community structure is related to the presence of SIL. Presence of SIL was also associated with a higher species richness (Chao 1). MaAsLiN analysis yielded independent associations between SIL/HPV status and an increase in the relative abundance Brachybacterium conglomeratum, as well as a decrease in Sphingobium yanoikuyae and Lactobacillus spp. We also identified independent associations between HPV-16, the most common HPV subtype linked to SIL, and Brachybacterium conglomeratum. Our work indicates that the presence of SIL and HPV infection is associated with important changes in the vaginal microbiome, some of which may be specific to this human population.IMPORTANCEHPV plays a critical role in cervical carcinogenesis but is not sufficient for cervical cancer development, indicating involvement of other factors. Vaginal microbiota is an important factor in controlling infections caused by HPV and depending on its composition it can modulate the microenvironment in vaginal mucosa against viral infection. Ethnic and sociodemographic factors influence differences in vaginal microbiome composition, which underlies the dysbiotic patterns linked to HPV infection and cervical cancer across different women populations. Here, we provide evidence for associations between vaginal microbiota patterns and HPV infection, linked to ethnic and sociodemographic factor. To our knowledge, this is the first report of Brevibacterium aureum and Brachybacterium conglomeratum species linked to HPV infection or SIL.


1998 ◽  
Vol 11 (4) ◽  
pp. 614-627 ◽  
Author(s):  
A. K. Patick ◽  
K. E. Potts

SUMMARY Currently, there are a number of approved antiviral agents for use in the treatment of viral infections. However, many instances exist in which the use of a second antiviral agent would be beneficial because it would allow the option of either an alternative or a combination therapeutic approach. Accordingly, virus-encoded proteases have emerged as new targets for antiviral intervention. Molecular studies have indicated that viral proteases play a critical role in the life cycle of many viruses by effecting the cleavage of high-molecular-weight viral polyprotein precursors to yield functional products or by catalyzing the processing of the structural proteins necessary for assembly and morphogenesis of virus particles. This review summarizes some of the important general features of virus-encoded proteases and highlights new advances and/or specific challenges that are associated with the research and development of viral protease inhibitors. Specifically, the viral proteases encoded by the herpesvirus, retrovirus, hepatitis C virus, and human rhinovirus families are discussed.


Author(s):  
Yanling Yang ◽  
Yang Liu ◽  
Wei Liu ◽  
Chunyang Li ◽  
Yuan Liu ◽  
...  

2016 ◽  
Vol 88 (9) ◽  
pp. 1646-1651 ◽  
Author(s):  
A. Pontillo ◽  
P. Bricher ◽  
V.N.C. Leal ◽  
S. Lima ◽  
P.R.E. Souza ◽  
...  

2014 ◽  
Vol 67 (8) ◽  
pp. 656-660 ◽  
Author(s):  
Sumit Sahni ◽  
Angelica M Merlot ◽  
Sukriti Krishan ◽  
Patric J Jansson ◽  
Des R Richardson

The BECN1 gene encodes the Beclin-1 protein, which is a well-established regulator of the autophagic pathway. It is a mammalian orthologue of the ATG6 gene in yeast and was one of the first identified mammalian autophagy-associated genes. Beclin-1 interacts with a number of binding partners in the cell which can lead to either activation (eg, via PI3KC3/Vps34, Ambra 1, UV radiation resistance-associated gene) or inhibition (eg, via Bcl-2, Rubicon) of the autophagic pathway. Apart from its role as a regulator of autophagy, it is also shown to effect important biological processes in the cell such as apoptosis and embryogenesis. Beclin-1 has also been implicated to play a critical role in the pathology of a variety of disease states including cancer, neurological disorders (eg, Alzheimer's disease, Parkinson's disease) and viral infections. Thus, understanding the functions of Beclin-1 and its interactions with other cellular components will aid in its development as an important therapeutic target for future drug development.


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