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Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer
CDCA3 is an essential regulator in cell mitosis and can regulate many physiological and pathological processes in the human body by stimulating certain proteins such as cell cycle regulatory proteins, transcription factors, and signal transduction molecules. Although several studies have shown that...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9448600/ https://www.ncbi.nlm.nih.gov/pubmed/36082153 http://dx.doi.org/10.1155/2022/4632453 |
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author | Xu, Yingkun Shen, Meiying Peng, Yang Liu, Li Tang, Lingfeng Yang, Ting Pu, Dongyao Tan, Wenhao Zhang, Wenjie Liu, Shengchun |
author_facet | Xu, Yingkun Shen, Meiying Peng, Yang Liu, Li Tang, Lingfeng Yang, Ting Pu, Dongyao Tan, Wenhao Zhang, Wenjie Liu, Shengchun |
author_sort | Xu, Yingkun |
collection | PubMed |
description | CDCA3 is an essential regulator in cell mitosis and can regulate many physiological and pathological processes in the human body by stimulating certain proteins such as cell cycle regulatory proteins, transcription factors, and signal transduction molecules. Although several studies have shown that dysregulation of CDCA3 is a common phenomenon in human cancers, no systematic pan-cancer analysis has been performed. In this study, we comprehensively investigated the role of CDCA3 in 33 human cancer types by utilizing multiple cancer-related databases and bioinformatics analysis tools, including TCGA, GTEx, GEPIA, TIMER, STRING, Metascape, and Cytoscape. Evidence from bioinformatics databases shows that CDCA3 is overexpressed in almost all human cancer types, and its overexpression is significantly associated with survival in patients with more than ten cancer types. CDCA3 expression positively correlates with immune cell infiltration levels in multiple human cancer types. Furthermore, the results of the GSEA analysis revealed that overexpression of CDCA3 may promote the malignant progression of cancer by activating various oncogenic signaling pathways in human cancers. In conclusion, our pan-cancer analysis provides a comprehensive overview of the oncogenic role of CDCA3 in multiple human cancer types, suggesting that CDCA3 may serve as a potential therapeutic target and prognostic biomarker in multiple human cancer types. |
format | Online Article Text |
id | pubmed-9448600 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-94486002022-09-07 Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer Xu, Yingkun Shen, Meiying Peng, Yang Liu, Li Tang, Lingfeng Yang, Ting Pu, Dongyao Tan, Wenhao Zhang, Wenjie Liu, Shengchun Biomed Res Int Research Article CDCA3 is an essential regulator in cell mitosis and can regulate many physiological and pathological processes in the human body by stimulating certain proteins such as cell cycle regulatory proteins, transcription factors, and signal transduction molecules. Although several studies have shown that dysregulation of CDCA3 is a common phenomenon in human cancers, no systematic pan-cancer analysis has been performed. In this study, we comprehensively investigated the role of CDCA3 in 33 human cancer types by utilizing multiple cancer-related databases and bioinformatics analysis tools, including TCGA, GTEx, GEPIA, TIMER, STRING, Metascape, and Cytoscape. Evidence from bioinformatics databases shows that CDCA3 is overexpressed in almost all human cancer types, and its overexpression is significantly associated with survival in patients with more than ten cancer types. CDCA3 expression positively correlates with immune cell infiltration levels in multiple human cancer types. Furthermore, the results of the GSEA analysis revealed that overexpression of CDCA3 may promote the malignant progression of cancer by activating various oncogenic signaling pathways in human cancers. In conclusion, our pan-cancer analysis provides a comprehensive overview of the oncogenic role of CDCA3 in multiple human cancer types, suggesting that CDCA3 may serve as a potential therapeutic target and prognostic biomarker in multiple human cancer types. Hindawi 2022-08-30 /pmc/articles/PMC9448600/ /pubmed/36082153 http://dx.doi.org/10.1155/2022/4632453 Text en Copyright © 2022 Yingkun Xu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Xu, Yingkun Shen, Meiying Peng, Yang Liu, Li Tang, Lingfeng Yang, Ting Pu, Dongyao Tan, Wenhao Zhang, Wenjie Liu, Shengchun Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title | Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title_full | Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title_fullStr | Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title_full_unstemmed | Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title_short | Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer |
title_sort | cell division cycle-associated protein 3 (cdca3) is a potential biomarker for clinical prognosis and immunotherapy in pan-cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9448600/ https://www.ncbi.nlm.nih.gov/pubmed/36082153 http://dx.doi.org/10.1155/2022/4632453 |
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