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Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils
At present, the impact of cuproptosis-related genes in the study of osteosarcoma is largely unknown. Genome-wide data of osteosarcoma and controls were downloaded from 3 different databases, and specific diagnostic models associated with cuproptosis in osteosarcoma were constructed by support vector...
Autores principales: | , , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10040405/ https://www.ncbi.nlm.nih.gov/pubmed/36967449 http://dx.doi.org/10.1038/s41598-023-32195-2 |
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author | Jiang, Jie Zhan, Xinli Wei, Jianxun Fan, Qie Li, Haowen Li, Hao Li, Shuzhen Zhao, Yong Yin, Guodong Tang, Lin Wu, Yongxiang Lan, Mindong Qin, Yijue Guo, Quan Xu, Weicheng Lu, Ling Yang, Yanwei Zhang, Yitian Qu, Haishun |
author_facet | Jiang, Jie Zhan, Xinli Wei, Jianxun Fan, Qie Li, Haowen Li, Hao Li, Shuzhen Zhao, Yong Yin, Guodong Tang, Lin Wu, Yongxiang Lan, Mindong Qin, Yijue Guo, Quan Xu, Weicheng Lu, Ling Yang, Yanwei Zhang, Yitian Qu, Haishun |
author_sort | Jiang, Jie |
collection | PubMed |
description | At present, the impact of cuproptosis-related genes in the study of osteosarcoma is largely unknown. Genome-wide data of osteosarcoma and controls were downloaded from 3 different databases, and specific diagnostic models associated with cuproptosis in osteosarcoma were constructed by support vector machines with artificial intelligence, random forest trees and LASSO regression. Differential analysis of immune cell infiltration was examined using routine blood data from 25,665 cases. Differential expression was examined using immunohistochemistry and PCR. PDHA1 and CDKN2A were obtained as specific cuproptosis-related biomarkers for osteosarcoma after artificial intelligence analysis. PDHA1, CDKN2A and neutrophils were differentially expressed in OS and control groups. PDHA1 and CDKN2A are significantly dysregulated in OS and are able to serve as biomarkers of OS. |
format | Online Article Text |
id | pubmed-10040405 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-100404052023-03-28 Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils Jiang, Jie Zhan, Xinli Wei, Jianxun Fan, Qie Li, Haowen Li, Hao Li, Shuzhen Zhao, Yong Yin, Guodong Tang, Lin Wu, Yongxiang Lan, Mindong Qin, Yijue Guo, Quan Xu, Weicheng Lu, Ling Yang, Yanwei Zhang, Yitian Qu, Haishun Sci Rep Article At present, the impact of cuproptosis-related genes in the study of osteosarcoma is largely unknown. Genome-wide data of osteosarcoma and controls were downloaded from 3 different databases, and specific diagnostic models associated with cuproptosis in osteosarcoma were constructed by support vector machines with artificial intelligence, random forest trees and LASSO regression. Differential analysis of immune cell infiltration was examined using routine blood data from 25,665 cases. Differential expression was examined using immunohistochemistry and PCR. PDHA1 and CDKN2A were obtained as specific cuproptosis-related biomarkers for osteosarcoma after artificial intelligence analysis. PDHA1, CDKN2A and neutrophils were differentially expressed in OS and control groups. PDHA1 and CDKN2A are significantly dysregulated in OS and are able to serve as biomarkers of OS. Nature Publishing Group UK 2023-03-26 /pmc/articles/PMC10040405/ /pubmed/36967449 http://dx.doi.org/10.1038/s41598-023-32195-2 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Jiang, Jie Zhan, Xinli Wei, Jianxun Fan, Qie Li, Haowen Li, Hao Li, Shuzhen Zhao, Yong Yin, Guodong Tang, Lin Wu, Yongxiang Lan, Mindong Qin, Yijue Guo, Quan Xu, Weicheng Lu, Ling Yang, Yanwei Zhang, Yitian Qu, Haishun Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title | Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title_full | Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title_fullStr | Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title_full_unstemmed | Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title_short | Artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, PDHA1, CDKN2A and neutrophils |
title_sort | artificial intelligence reveals dysregulation of osteosarcoma and cuproptosis-related biomarkers, pdha1, cdkn2a and neutrophils |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10040405/ https://www.ncbi.nlm.nih.gov/pubmed/36967449 http://dx.doi.org/10.1038/s41598-023-32195-2 |
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