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Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma
Minichromosome maintenance (MCM) family members are a group of genes involved in regulating DNA replication and cell division and have been identified as oncogenes in various cancer types. Several experimental studies have suggested that MCMs are dysregulated in endometrial carcinoma (EC). However,...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8685644/ https://www.ncbi.nlm.nih.gov/pubmed/34859821 http://dx.doi.org/10.1042/BSR20211719 |
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author | Lan, Hua Yuan, Jing Chen, Xingyu Liu, Chu Guo, Xiaohui Wang, Xinyu Song, Jiarui Cao, Ke Xiao, Songshu |
author_facet | Lan, Hua Yuan, Jing Chen, Xingyu Liu, Chu Guo, Xiaohui Wang, Xinyu Song, Jiarui Cao, Ke Xiao, Songshu |
author_sort | Lan, Hua |
collection | PubMed |
description | Minichromosome maintenance (MCM) family members are a group of genes involved in regulating DNA replication and cell division and have been identified as oncogenes in various cancer types. Several experimental studies have suggested that MCMs are dysregulated in endometrial carcinoma (EC). However, the expression pattern, clinical value and functions of different MCMs have yet to be analyzed systematically and comprehensively. We analyzed expression, survival rate, DNA alteration, PPT network, GGI network, functional enrichment cancer hallmarks and drug sensitivity of MCMs in patients with EC based on diverse datasets, including Oncomine, GEPIA, Kaplan–Meier Plotter, HPA, Sangerbox and GSCALite databases. The results indicated that most MCM members were increased in EC and showed a prognostic value in survival analysis, which were considerately well in terms of PFS and OS prognostic prediction. Importantly, functional enrichment, PPI network and GGI network suggested that MCMs interact with proteins related to DNA replication and cell division, which may be the mechanism of MCM promote EC progression. Further data mining illustrated that MCMs have broad DNA hypomethylation levels and high levels of copy number aberrations in tumor tissue samples, which may be the mechanism causing the high expression level of MCMs. Moreover, MCM2 can activate or suppress diverse cancer-related pathways and is implicated in EC drug sensitivity. Taking together, our findings illustrate the expression pattern, clinical value and function of MCMs in EC and imply that MCMs are potential targets for precision therapy and new biomarkers for the prognosis of patients with EC. |
format | Online Article Text |
id | pubmed-8685644 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86856442021-12-21 Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma Lan, Hua Yuan, Jing Chen, Xingyu Liu, Chu Guo, Xiaohui Wang, Xinyu Song, Jiarui Cao, Ke Xiao, Songshu Biosci Rep Bioinformatics Minichromosome maintenance (MCM) family members are a group of genes involved in regulating DNA replication and cell division and have been identified as oncogenes in various cancer types. Several experimental studies have suggested that MCMs are dysregulated in endometrial carcinoma (EC). However, the expression pattern, clinical value and functions of different MCMs have yet to be analyzed systematically and comprehensively. We analyzed expression, survival rate, DNA alteration, PPT network, GGI network, functional enrichment cancer hallmarks and drug sensitivity of MCMs in patients with EC based on diverse datasets, including Oncomine, GEPIA, Kaplan–Meier Plotter, HPA, Sangerbox and GSCALite databases. The results indicated that most MCM members were increased in EC and showed a prognostic value in survival analysis, which were considerately well in terms of PFS and OS prognostic prediction. Importantly, functional enrichment, PPI network and GGI network suggested that MCMs interact with proteins related to DNA replication and cell division, which may be the mechanism of MCM promote EC progression. Further data mining illustrated that MCMs have broad DNA hypomethylation levels and high levels of copy number aberrations in tumor tissue samples, which may be the mechanism causing the high expression level of MCMs. Moreover, MCM2 can activate or suppress diverse cancer-related pathways and is implicated in EC drug sensitivity. Taking together, our findings illustrate the expression pattern, clinical value and function of MCMs in EC and imply that MCMs are potential targets for precision therapy and new biomarkers for the prognosis of patients with EC. Portland Press Ltd. 2021-12-17 /pmc/articles/PMC8685644/ /pubmed/34859821 http://dx.doi.org/10.1042/BSR20211719 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Bioinformatics Lan, Hua Yuan, Jing Chen, Xingyu Liu, Chu Guo, Xiaohui Wang, Xinyu Song, Jiarui Cao, Ke Xiao, Songshu Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title | Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title_full | Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title_fullStr | Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title_full_unstemmed | Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title_short | Multiomics profiling of the expression and prognosis of MCMs in endometrial carcinoma |
title_sort | multiomics profiling of the expression and prognosis of mcms in endometrial carcinoma |
topic | Bioinformatics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8685644/ https://www.ncbi.nlm.nih.gov/pubmed/34859821 http://dx.doi.org/10.1042/BSR20211719 |
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