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Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility
BACKGROUND: Cervical cancer is the fourth most common and fatal tumor among women worldwide. The Wnt/β-catenin signaling pathway was etiologically involved in the cervical cancer model. Herein, we aimed to investigate whether germline genetic variations within the Wnt/β-catenin pathway can be geneti...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247596/ https://www.ncbi.nlm.nih.gov/pubmed/32547159 http://dx.doi.org/10.2147/PGPM.S248548 |
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author | Wang, Bingqi Wang, Min Li, Xianping Yang, Min Liu, Lei |
author_facet | Wang, Bingqi Wang, Min Li, Xianping Yang, Min Liu, Lei |
author_sort | Wang, Bingqi |
collection | PubMed |
description | BACKGROUND: Cervical cancer is the fourth most common and fatal tumor among women worldwide. The Wnt/β-catenin signaling pathway was etiologically involved in the cervical cancer model. Herein, we aimed to investigate whether germline genetic variations within the Wnt/β-catenin pathway can be genetic risk factors of cervical cancer. PATIENTS AND METHODS: A total of 305 samples (147 patients, 158 controls) were included. Eight genetic variations located in APC (rs454886), GSK3β (rs3755557), CTNNB1 (rs11564475, rs1798802, rs3864004, rs2293303, and rs4135385), and TCF7L2 (rs7903146) were genotyped via Sanger sequencing. The χ(2) test and non-conditional logistic regression were used in the single-locus analysis. Gene–gene interactions and haplotype construction in case–control samples were performed by the GMDR method and Haploview software, respectively. RESULTS: The frequency of CTNNB1 rs1798802 GA+AA genotype was significantly lower in cervical cancer patients adjusted for age (OR=0.626, 95% CI=0.398–0.984). The mutant alleles of rs3864004 (A) and rs2293303 (T) located in CTNNB1 showed 1.513 (1.038–2.207), and 1.654 (1.020–2.683) fold increased risk of cervical cancer, respectively. Haplotype analysis showed no association between haplotypes of the CTNNB1 gene and cervical cancer risk. No significant contribution of interactions among genes in the Wnt pathway was identified. CONCLUSION: We concluded that the genetic variants in the CTNNB1 gene might contribute to the development of cervical cancer. |
format | Online Article Text |
id | pubmed-7247596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-72475962020-06-15 Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility Wang, Bingqi Wang, Min Li, Xianping Yang, Min Liu, Lei Pharmgenomics Pers Med Original Research BACKGROUND: Cervical cancer is the fourth most common and fatal tumor among women worldwide. The Wnt/β-catenin signaling pathway was etiologically involved in the cervical cancer model. Herein, we aimed to investigate whether germline genetic variations within the Wnt/β-catenin pathway can be genetic risk factors of cervical cancer. PATIENTS AND METHODS: A total of 305 samples (147 patients, 158 controls) were included. Eight genetic variations located in APC (rs454886), GSK3β (rs3755557), CTNNB1 (rs11564475, rs1798802, rs3864004, rs2293303, and rs4135385), and TCF7L2 (rs7903146) were genotyped via Sanger sequencing. The χ(2) test and non-conditional logistic regression were used in the single-locus analysis. Gene–gene interactions and haplotype construction in case–control samples were performed by the GMDR method and Haploview software, respectively. RESULTS: The frequency of CTNNB1 rs1798802 GA+AA genotype was significantly lower in cervical cancer patients adjusted for age (OR=0.626, 95% CI=0.398–0.984). The mutant alleles of rs3864004 (A) and rs2293303 (T) located in CTNNB1 showed 1.513 (1.038–2.207), and 1.654 (1.020–2.683) fold increased risk of cervical cancer, respectively. Haplotype analysis showed no association between haplotypes of the CTNNB1 gene and cervical cancer risk. No significant contribution of interactions among genes in the Wnt pathway was identified. CONCLUSION: We concluded that the genetic variants in the CTNNB1 gene might contribute to the development of cervical cancer. Dove 2020-05-20 /pmc/articles/PMC7247596/ /pubmed/32547159 http://dx.doi.org/10.2147/PGPM.S248548 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wang, Bingqi Wang, Min Li, Xianping Yang, Min Liu, Lei Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title | Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title_full | Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title_fullStr | Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title_full_unstemmed | Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title_short | Variations in the Wnt/β-Catenin Pathway Key Genes as Predictors of Cervical Cancer Susceptibility |
title_sort | variations in the wnt/β-catenin pathway key genes as predictors of cervical cancer susceptibility |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247596/ https://www.ncbi.nlm.nih.gov/pubmed/32547159 http://dx.doi.org/10.2147/PGPM.S248548 |
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