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Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis

Ulcerative colitis (UC) is a chronic, highly heterogeneous intestinal inflammation with changes in epithelial function and tissue damage. However, the pathogenesis is still unclear between active UC and inactive UC. Herein, weighted gene co‐expression network analysis was applied to explore the gene...

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Autores principales: Wang, Haizhou, Zhang, Meng, Zhang, Mengna, Wang, Fan, Liu, Jing, Zhao, Qiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412415/
https://www.ncbi.nlm.nih.gov/pubmed/32570281
http://dx.doi.org/10.1111/jcmm.15517
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author Wang, Haizhou
Zhang, Meng
Zhang, Mengna
Wang, Fan
Liu, Jing
Zhao, Qiu
author_facet Wang, Haizhou
Zhang, Meng
Zhang, Mengna
Wang, Fan
Liu, Jing
Zhao, Qiu
author_sort Wang, Haizhou
collection PubMed
description Ulcerative colitis (UC) is a chronic, highly heterogeneous intestinal inflammation with changes in epithelial function and tissue damage. However, the pathogenesis is still unclear between active UC and inactive UC. Herein, weighted gene co‐expression network analysis was applied to explore the gene modules related to active UC. Gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA) were used to further investigate the underlying mechanism of selected genes. We found that in the blue module (r = −.72), carboxypeptidase A6 (CPA6) was chosen to validate because of its high intra‐modular connectivity and module membership. In the test sets, the expression level of CPA6 was down‐regulated in active UC compared with inactive UC and normal colon. Furthermore, CPA6 expression was decreased primarily in the descending colon and only in mucosa affected by active UC. The receiver operating characteristic curve indicated that CPA6 expression had a performed well in diagnosing active UC from inactive UC (area under the curve = 0.99). Importantly, anti‐tumour necrosis factor (TNF) treatment (infliximab and golimumab) significantly increased the CPA6 expression. Finally, GSEA and GSVA found that extracellular matrix receptor, inflammatory response and epithelial‐mesenchymal transition were highly enriched in active UC with low CPA6 expression. In conclusion, CPA6 was identified and validated as a novel potential biomarker for predicting the occurrence of active UC, probably through regulating extracellular matrix or immune response.
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spelling pubmed-74124152020-08-10 Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis Wang, Haizhou Zhang, Meng Zhang, Mengna Wang, Fan Liu, Jing Zhao, Qiu J Cell Mol Med Original Articles Ulcerative colitis (UC) is a chronic, highly heterogeneous intestinal inflammation with changes in epithelial function and tissue damage. However, the pathogenesis is still unclear between active UC and inactive UC. Herein, weighted gene co‐expression network analysis was applied to explore the gene modules related to active UC. Gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA) were used to further investigate the underlying mechanism of selected genes. We found that in the blue module (r = −.72), carboxypeptidase A6 (CPA6) was chosen to validate because of its high intra‐modular connectivity and module membership. In the test sets, the expression level of CPA6 was down‐regulated in active UC compared with inactive UC and normal colon. Furthermore, CPA6 expression was decreased primarily in the descending colon and only in mucosa affected by active UC. The receiver operating characteristic curve indicated that CPA6 expression had a performed well in diagnosing active UC from inactive UC (area under the curve = 0.99). Importantly, anti‐tumour necrosis factor (TNF) treatment (infliximab and golimumab) significantly increased the CPA6 expression. Finally, GSEA and GSVA found that extracellular matrix receptor, inflammatory response and epithelial‐mesenchymal transition were highly enriched in active UC with low CPA6 expression. In conclusion, CPA6 was identified and validated as a novel potential biomarker for predicting the occurrence of active UC, probably through regulating extracellular matrix or immune response. John Wiley and Sons Inc. 2020-06-22 2020-08 /pmc/articles/PMC7412415/ /pubmed/32570281 http://dx.doi.org/10.1111/jcmm.15517 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Wang, Haizhou
Zhang, Meng
Zhang, Mengna
Wang, Fan
Liu, Jing
Zhao, Qiu
Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title_full Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title_fullStr Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title_full_unstemmed Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title_short Carboxypeptidase A6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
title_sort carboxypeptidase a6 was identified and validated as a novel potential biomarker for predicting the occurrence of active ulcerative colitis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412415/
https://www.ncbi.nlm.nih.gov/pubmed/32570281
http://dx.doi.org/10.1111/jcmm.15517
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