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ORIGINAL RESEARCH article

Front. Oncol.

Sec. Cancer Genetics

Volume 15 - 2025 | doi: 10.3389/fonc.2025.1655143

This article is part of the Research TopicDeciphering molecular mechanisms behind tumor heterogeneity features by using nucleic acid-based technologiesView all 3 articles

Transcriptome Analyses Identify Deregulated 10 Hub Genes and Essential Molecular Mechanisms in Early Onset Colorectal Cancer

Provisionally accepted
Hieu Duc NguyenHieu Duc Nguyen1,2Ming-Jenn ChenMing-Jenn Chen3,4Chung Ying LeeChung Ying Lee5,6,7Yi-Chun NiYi-Chun Ni2Ke Xin YeeKe Xin Yee2Yung-Fu WuYung-Fu Wu8*Kuen-Haur LeeKuen-Haur Lee1,10,2,7,9*
  • 1Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University-Shuangho Campus, New Taipei City, Taiwan
  • 2PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University-Shuangho Campus, New Taipei City, Taiwan
  • 3Department of Surgery, Chi Mei Medical Center, Tainan City, Taiwan
  • 4Department of Sports Management, College of Leisure and Recreation Management, Chia Nan University of Pharmacy and Science, Tainan City, Taiwan
  • 5Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital Ministry of Health and Welfare, New Taipei City, Taiwan
  • 6Gastroenterology and Hepatology, Taipei Medical University School of Medicine, Taipei City, Taiwan
  • 7TMU Research Center for Digestive Medicine, Taipei Medical University, Taipei City, Taiwan
  • 8National Defense Medical Center, School of Medicine, Department of Medical Research, Tri-Service General Hospital, Taipei City, Taiwan
  • 9Cancer Center, Wan Fang Hospital, Taipei Medical University, Taipei City, Taiwan
  • 10TMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei City, Taiwan

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The rapid increase in Early-Onset Colorectal Cancer (EoCRC) case numbers in recent years indicated an urgent need to identify the essential mechanisms and makers for EoCRC diagnosis and treatment. Therefore, this study aimed to analyze the metadata to overcome the limitation of the sample number of previous EoCRC research and to identify central mechanisms and genes that are crucial for early-onset colorectal cancer. This study employed statistical analysis of data from the cBioPortal and GEPIA databases to identify overexpressed EoCRC genes. Using a protein-protein interaction map, it identified hub genes. The function of these genes was clarified via risk model, survival, and cell model analysis. The results of clinical data analysis showed an increased rate of late-stage and a lower overall survival of the EoCRC cohort. 953 enriched gene samples were detected in EoCRC and 89 genes were identified as EOCRC overexpression genes. From the protein-protein interactions among 53 genes, the top ten hub genes showed potential for EoCRC diagnosis and prognosis by linking gene expression to diagnosis and survival analysis data. The knockdown of four selected hub gene in cell model identified the association of EoCRC over expression hub genes with tumor development and suggested their role in mTOR signaling, cell cycle and apoptosis regulation. In summary, the study analyzed molecular and clinical data to identify hub genes associated with cancer prognosis in EoCRC patients. These genes may serve as targets for diagnosis and treatment.

Keywords: Early-onset colorectal cancer, metadata, Transcriptome, Risk model, EoCRC cell model, Cell Cycle, Apoptosis, EOCRC

Received: 27 Jun 2025; Accepted: 08 Sep 2025.

Copyright: © 2025 Nguyen, Chen, Lee, Ni, Yee, Wu and Lee. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Yung-Fu Wu, National Defense Medical Center, School of Medicine, Department of Medical Research, Tri-Service General Hospital, Taipei City, Taiwan
Kuen-Haur Lee, Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University-Shuangho Campus, New Taipei City, Taiwan

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Supplementary Material