Identification of Potential Key Genes and Pathways in Early-Onset Colorectal Cancer Through Bioinformatics Analysis

Author:

Zhao Bin1,Baloch Zulqarnain2ORCID,Ma Yunhan1,Wan Zheng1,Huo Yani1,Li Fujun3,Zhao Yilin14

Affiliation:

1. Medical College of Xiamen University, Xiamen, Fujian, China

2. College of Veterinary Medicine, South China Agricultural University, Guangzhou, China

3. The Department of Anesthesiology, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China

4. Department of Oncology and Vascular Interventional Radiology, Zhongshan Hospital affiliated of Xiamen University, Xiamen, Fujian, China

Abstract

This study was designed to identify the potential key protein interaction networks, genes, and correlated pathways in early-onset colorectal cancer (CRC) via bioinformatics methods. We selected microarray data GSE4107 consisting 12 patient’s colonic mucosa and 10 healthy control mucosa; initially, the GSE4107 were downloaded and analyzed using limma package to identify differentially expressed genes (DEGs). A total of 131 DEGs consisting of 108 upregulated genes and 23 downregulated genes of patients in early-onset CRC were selected by the criteria of adjusted P values <.01 and |log2 fold change (FC)| ≥ 2. The gene ontology functional enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were accomplished to view the biological process, cellular components, molecular function, and the KEGG pathways of DEGs. Finally, protein–protein interactions (PPIs) were constructed, and the hub protein module was identified. Genes such as ACTA2, ACTG2, MYH11, CALD1, MYL9, TPM2, and LMOD1 were strongly implicated in CRC. In summary, in this study, we indicated that molecular mechanisms were involved in muscle contraction and vascular smooth muscle contraction signaling pathway, which improve our understanding of CRC and could be used as new therapeutic targets for CRC.

Publisher

SAGE Publications

Subject

Oncology,Hematology,General Medicine

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