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Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing
Human glucose-6-phosphate dehydrogenase (G6PD) is a crucial enzyme in the pentose phosphate pathway, and serves an important role in biosynthesis and the redox balance. G6PD deficiency is a major cause of neonatal jaundice and acute hemolyticanemia, and recently, G6PD has been associated with diseas...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562079/ https://www.ncbi.nlm.nih.gov/pubmed/28627690 http://dx.doi.org/10.3892/mmr.2017.6785 |
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author | Chen, Long Zhang, Chunhua Wang, Yanling Li, Yuqian Han, Qiaoqiao Yang, Huixin Zhu, Yuechun |
author_facet | Chen, Long Zhang, Chunhua Wang, Yanling Li, Yuqian Han, Qiaoqiao Yang, Huixin Zhu, Yuechun |
author_sort | Chen, Long |
collection | PubMed |
description | Human glucose-6-phosphate dehydrogenase (G6PD) is a crucial enzyme in the pentose phosphate pathway, and serves an important role in biosynthesis and the redox balance. G6PD deficiency is a major cause of neonatal jaundice and acute hemolyticanemia, and recently, G6PD has been associated with diseases including inflammation and cancer. The aim of the present study was to conduct a search of the National Center for Biotechnology Information PubMed library for articles discussing G6PD. Genes that were identified to be associated with G6PD were recorded, and the frequency at which each gene appeared was calculated. Gene ontology (GO), pathway and network analyses were then performed. A total of 98 G6PD-associated genes and 33 microRNAs (miRNAs) that potentially regulate G6PD were identified. The 98 G6PD-associated genes were then sub-classified into three functional groups by GO analysis, followed by analysis of function, pathway, network, and disease association. Out of the 47 signaling pathways identified, seven were significantly correlated with G6PD-associated genes. At least two out of four independent programs identified the 33 miRNAs that were predicted to target G6PD. miR-1207-5P, miR-1 and miR-125a-5p were predicted by all four software programs to target G6PD. The results of the present study revealed that dysregulation of G6PD was associated with cancer, autoimmune diseases, and oxidative stress-induced disorders. These results revealed the potential roles of G6PD-regulated signaling and metabolic pathways in the etiology of these diseases. |
format | Online Article Text |
id | pubmed-5562079 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-55620792017-10-23 Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing Chen, Long Zhang, Chunhua Wang, Yanling Li, Yuqian Han, Qiaoqiao Yang, Huixin Zhu, Yuechun Mol Med Rep Articles Human glucose-6-phosphate dehydrogenase (G6PD) is a crucial enzyme in the pentose phosphate pathway, and serves an important role in biosynthesis and the redox balance. G6PD deficiency is a major cause of neonatal jaundice and acute hemolyticanemia, and recently, G6PD has been associated with diseases including inflammation and cancer. The aim of the present study was to conduct a search of the National Center for Biotechnology Information PubMed library for articles discussing G6PD. Genes that were identified to be associated with G6PD were recorded, and the frequency at which each gene appeared was calculated. Gene ontology (GO), pathway and network analyses were then performed. A total of 98 G6PD-associated genes and 33 microRNAs (miRNAs) that potentially regulate G6PD were identified. The 98 G6PD-associated genes were then sub-classified into three functional groups by GO analysis, followed by analysis of function, pathway, network, and disease association. Out of the 47 signaling pathways identified, seven were significantly correlated with G6PD-associated genes. At least two out of four independent programs identified the 33 miRNAs that were predicted to target G6PD. miR-1207-5P, miR-1 and miR-125a-5p were predicted by all four software programs to target G6PD. The results of the present study revealed that dysregulation of G6PD was associated with cancer, autoimmune diseases, and oxidative stress-induced disorders. These results revealed the potential roles of G6PD-regulated signaling and metabolic pathways in the etiology of these diseases. D.A. Spandidos 2017-08 2017-06-15 /pmc/articles/PMC5562079/ /pubmed/28627690 http://dx.doi.org/10.3892/mmr.2017.6785 Text en Copyright: © Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Chen, Long Zhang, Chunhua Wang, Yanling Li, Yuqian Han, Qiaoqiao Yang, Huixin Zhu, Yuechun Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title | Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title_full | Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title_fullStr | Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title_full_unstemmed | Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title_short | Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
title_sort | data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562079/ https://www.ncbi.nlm.nih.gov/pubmed/28627690 http://dx.doi.org/10.3892/mmr.2017.6785 |
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