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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

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CDK1, CCNB1, CDC20, BUB1, MAD2L1, MCM3, BUB1B, MCM2, and RFC4 May Be Potential Therapeutic Targets for Hepatocellular

Wan-Xia Yang1, Yun-Yan Pan1, Chong-Ge You1

  • 1Laboratory Medicine Center, Lanzhou University Second Hospital, Lanzhou, Gansu 730030, China.

Biomed Research International
|November 19, 2019
PubMed

Insights

This study identified nine key genes (CDK1, CCNB1, CDC20, BUB1, MAD2L1, MCM3, BUB1B, MCM2, RFC4) that are highly expressed in hepatocellular carcinoma (HCC) and linked to poor patient survival. These genes represent potential therapeutic targets for HCC treatment.

Area of Science:

  • Oncology
  • Bioinformatics
  • Molecular Biology

Background:

  • Hepatocellular carcinoma (HCC) is a deadly cancer with complex genetic underpinnings.
  • Identifying specific genes driving HCC development is crucial for effective treatment strategies.

Purpose of the Study:

  • To identify differentially expressed genes (DEGs) in HCC.
  • To provide a bioinformatics foundation for understanding HCC occurrence, prevention, and treatment.

Main Methods:

  • Utilized R language to analyze gene expression data from HCC and normal tissues across multiple datasets (GSE102079, GSE121248, GSE84402, GSE60502).
  • Performed Gene Ontology (GO) and KEGG pathway analysis using DAVID, constructed protein-protein interaction (PPI) networks with STRING, and identified hub genes via Cytoscape.
  • Validated hub gene expression and clinical correlations using GEPIA, UALCAN, Oncomine, HPA, and LinkedOmics databases, with transcription factor (TF) analysis performed using NetworkAnalyst.

Main Results:

  • Identified 591 overlapping upregulated genes in HCC, associated with cell cycle, DNA replication, pyrimidine metabolism, and p53 signaling pathways.
  • Nine hub genes (CDK1, CCNB1, CDC20, BUB1, MAD2L1, MCM3, BUB1B, MCM2, RFC4) were significantly associated with poor HCC patient survival and highly expressed in tumor tissues.
  • These genes showed correlations with overall survival, pathologic stage, T stage, race, and age of onset.
  • MYBL2, KDM5B, MYC, SOX2, and E2F4 were identified as key transcription factors regulating these hub genes.

Conclusions:

  • The nine identified hub genes are significantly overexpressed in HCC and predict poor survival, indicating their potential as therapeutic targets.
  • This study provides valuable bioinformatics insights into HCC pathogenesis and potential clinical applications.

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