Abstract
The underlying causes of esophageal cancer (EC) are unknown. To explore the molecular mechanisms that lead to EC, gene expression profiles of large cohorts of patients with EC were obtained from The Cancer Genome Atlas and the Gene Expression Omnibus (GEO) databases (GSE5364, GSE20347 and GSE23400). The present study identified 83 upregulated and 22 downregulated genes between EC and normal tissue using R statistical software and the GEO2R web tool. The Database for Annotation, Visualization and Integrated Discovery was used to identify the associated pathways, and for functional annotation of the differentially expressed genes (DEGs). Protein-protein interactions of these DEGs were analyzed based on the Search Tool for the Retrieval of Interacting Genes database, and hub genes were visualized using Cytoscape software. An online Kaplan-Meier plotter survival analysis tool was utilized to evaluate the prognostic value of hub gene expression in patients with EC. Further analysis of an additional dataset from GEO (GSE21293) revealed that these genes were associated with infiltration and metastasis in EC. In addition, the Gene Expression Profiling Interactive Analysis tool was used to evaluate expression levels of hub genes in patients with EC for different pathological stages. The Ualcan analysis tool was used to evaluate the expression levels of hub genes for different histological types. Overall, ubiquitin conjugating enzyme E2 C, cyclin dependent kinase inhibitor 3, CDC28 protein kinase regulatory subunit 2, kinesin family member 20A (KIF20A) and RAD51 associated protein 1 (RAD51AP1) were upregulated in EC tissues compared with normal tissues, and upregulation of these genes was a poor prognostic factor for patients with EC, indicating that these genes may mediate EC cell infiltration and metastasis. Among the hub genes, KIF-20A had potential value for predicting the pathological stage of EC. KIF20A and RAD51AP1 were more informative biomarkers of esophageal squamous cell carcinoma. Further studies are required to explore the value of these genes in the treatment of EC.
Highlights
Gastrointestinal cancer is a major health problem with 4.8 million new cases and 3.4 million mortality cases reported worldwide in 2018 [1]
Through comprehensive analysis of Esophageal cancer (EC) gene expression profiles in the The Cancer Genome Atlas (TCGA) database and three datasets from the Gene Expression Omnibus (GEO) database, a total of 105 differentially expressed genes (DEGs) were iden‐ tified between EC and normal tissues
These DEGs were associated with the proliferation of tumor cells and cell matrix remodeling, which revealed that cell cycle disorders, and invasion and migration were important mecha‐ nisms leading to the development of EC
Summary
Gastrointestinal cancer is a major health problem with 4.8 million new cases and 3.4 million mortality cases reported worldwide in 2018 [1]. Esophageal cancer (EC) is an aggres‐ sive malignancy originating in the gastrointestinal tract, with the eighth highest cancer incidence worldwide, and is the sixth most frequent cause of cancer‐associated mortality between 1995 and 2009 [2]. EC is more common in Asia than in other parts of the world [1], and EC incidence rate in China ranks first in the world, and is >35.0% higher than in the rest of the world. ESCC is the major type of EC found in China [3]. The primary treatment for EC is surgery; due to the absence of early symptoms, most patients are diagnosed with advanced EC, which results in high mortality rate [3].
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