Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues

Abstract Background Colorectal cancer (CRC) is one of the most common malignancies and the second most common cause of cancer-related mortality worldwide. Despite extensive research, the mechanism underlying CRC development remains unclear. This study aimed to understand the development and progress...

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Main Authors: Soo Bin Lee, Young Seon Noh, Ji-Wook Moon, Soohyun Sim, Sung Won Han, Eun Sun Kim, Ji-Yun Lee
Format: Article
Language:English
Published: BioMed Central 2025-06-01
Series:Genomics & Informatics
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Online Access:https://doi.org/10.1186/s44342-025-00046-3
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author Soo Bin Lee
Young Seon Noh
Ji-Wook Moon
Soohyun Sim
Sung Won Han
Eun Sun Kim
Ji-Yun Lee
author_facet Soo Bin Lee
Young Seon Noh
Ji-Wook Moon
Soohyun Sim
Sung Won Han
Eun Sun Kim
Ji-Yun Lee
author_sort Soo Bin Lee
collection DOAJ
description Abstract Background Colorectal cancer (CRC) is one of the most common malignancies and the second most common cause of cancer-related mortality worldwide. Despite extensive research, the mechanism underlying CRC development remains unclear. This study aimed to understand the development and progression of CRC. Methods Gene network analysis of tumors with their paired normal tissues was performed using the differentially expressed genes dataset for CRC from the Cancer Genome Atlas. Further investigation of the regulatory relationship between hub genes and tumor development was conducted by protein–protein interaction network, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway analyses using the selected hub genes. Results The network was more centered, and a common hub as well as a hub of hub genes were more connected to each other in the tumor than in the normal tissue, indicating changes in the network from normal to tumor. Eight downregulated and two upregulated hub genes (CDK1 and KIF11) in the tumor were identified. Further, the regulatory pathway was altered, especially in cell cycle and cell division. All R implementation codes are available on the journal website as supplementary materials. Conclusions Our findings may help understand the biological processes underlying tumor development and progression and suggest CDK1 and KIF11 as possible key molecules in the development of CRC.
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spelling doaj-art-6c3e5b19dcf24d53938b3f829d55ec5d2025-08-20T03:10:28ZengBioMed CentralGenomics & Informatics2234-07422025-06-0123111310.1186/s44342-025-00046-3Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissuesSoo Bin Lee0Young Seon Noh1Ji-Wook Moon2Soohyun Sim3Sung Won Han4Eun Sun Kim5Ji-Yun Lee6School of Industrial and Management Engineering, Korea UniversitySchool of Industrial and Management Engineering, Korea UniversityBK21Plus Medical Science, Department of Anatomy, Korea University College of MedicineDepartment of Biomedical Science, Korea University College of MedicineSchool of Industrial and Management Engineering, Korea UniversityDepartment of Internal Medicine, Korea University College of MedicineDepartment of Pathology, Korea University College of MedicineAbstract Background Colorectal cancer (CRC) is one of the most common malignancies and the second most common cause of cancer-related mortality worldwide. Despite extensive research, the mechanism underlying CRC development remains unclear. This study aimed to understand the development and progression of CRC. Methods Gene network analysis of tumors with their paired normal tissues was performed using the differentially expressed genes dataset for CRC from the Cancer Genome Atlas. Further investigation of the regulatory relationship between hub genes and tumor development was conducted by protein–protein interaction network, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway analyses using the selected hub genes. Results The network was more centered, and a common hub as well as a hub of hub genes were more connected to each other in the tumor than in the normal tissue, indicating changes in the network from normal to tumor. Eight downregulated and two upregulated hub genes (CDK1 and KIF11) in the tumor were identified. Further, the regulatory pathway was altered, especially in cell cycle and cell division. All R implementation codes are available on the journal website as supplementary materials. Conclusions Our findings may help understand the biological processes underlying tumor development and progression and suggest CDK1 and KIF11 as possible key molecules in the development of CRC.https://doi.org/10.1186/s44342-025-00046-3Colorectal cancerNetwork analysisCDK1KIF11
spellingShingle Soo Bin Lee
Young Seon Noh
Ji-Wook Moon
Soohyun Sim
Sung Won Han
Eun Sun Kim
Ji-Yun Lee
Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
Genomics & Informatics
Colorectal cancer
Network analysis
CDK1
KIF11
title Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
title_full Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
title_fullStr Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
title_full_unstemmed Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
title_short Gene expression network analysis identified CDK1 and KIF11 as possible key molecules in the development of colorectal cancer from normal tissues
title_sort gene expression network analysis identified cdk1 and kif11 as possible key molecules in the development of colorectal cancer from normal tissues
topic Colorectal cancer
Network analysis
CDK1
KIF11
url https://doi.org/10.1186/s44342-025-00046-3
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