Abstract
Background: Esophageal cancer (EC) is one of the deadliest cancers in the world. However, the mechanism that drives the evolution of EC is still unclear. On this basis, we identified the key genes and molecular pathways that may be related to the progression of esophageal adenocarcinoma and squamous cell carcinoma to find potential markers or therapeutic targets.Methods: GSE26886 were obtained from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) among normal samples, EA, and squamous cell carcinoma were determined using R software. Then, potential functions of DEGs were determined using the Database for Annotation, Visualization and Integrated Discovery (DAVID). The STRING software was used to identify the most important modules in the protein–protein interaction (PPI) network. The expression levels of hub genes were confirmed using UALCAN database. Kaplan–Meier plotters were used to confirm the correlation between hub genes and outcomes in EC.Results: In this study, we identified 1,098 genes induced in esophageal adenocarcinoma (EA) and esophageal squamous cell carcinoma (ESCC), and 669 genes were reduced in EA and ESCC, suggesting that these genes may play an important role in the occurrence and development of EC tumors. Bioinformatics analysis showed that these genes were involved in cell cycle regulation and p53 and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. In addition, we identified 147 induced genes and 130 reduced genes differentially expressed in EA and ESCC. The expression of ESCC in the EA group was different from that in the control group. By PPI network analysis, we identified 10 hub genes, including GNAQ, RGS5, MAPK1, ATP1B1, HADHA, HSDL2, SLC25A20, ACOX1, SCP2, and NLN. TCGA validation showed that these genes were present in the dysfunctional samples between EC and normal samples and between EA and ESCC. Kaplan–Meier analysis showed that MAPK1, ACOX1, SCP2, and NLN were associated with overall survival in patients with ESCC and EA.Conclusions: In this study, we identified a series of DEGs between EC and normal samples and between EA and ESCC samples. We also identified 10 key genes involved in the EC process. We believe that this study may provide a new biomarker for the prognosis of EA and ESCC.
Highlights
According to the cancer statistics in 2018, the mortality rate of esophageal cancer ranks sixth among all tumors all over the world (Bray et al, 2018; Gu et al, 2020b)
We revealed 1,098 common induced genes in both esophageal adenocarcinoma (EA) and esophageal squamous cell carcinoma (ESCC) (Figure 1E) and 669 common reduced genes in both EA and ESCC compared to normal samples (Figure 1F), suggesting that these genes may have a crucial role in the tumorigenesis and progression of both EA and ESCC
We found that 1,669 ESCC-specific upregulated, 1,434 EA-specific upregulated, 1,437 ESCC-specific downregulated, and 799 EAspecific downregulated genes, further confirming that that there are significant differences in the pathogenesis between EA and ESCC (Figures 1E,F)
Summary
According to the cancer statistics in 2018, the mortality rate of esophageal cancer ranks sixth among all tumors all over the world (Bray et al, 2018; Gu et al, 2020b). Esophageal carcinoma (EC) is divided into esophageal adenocarcinoma (EA) and esophageal squamous cell carcinoma (ESCC) ( et al, 2020). EA occurs in the lower portion of the esophagus and arises as a consequence of persistent gastroesophageal reflux from areas with specialized intestinal metaplasia in Barrett’s esophagus (Gindea et al, 2014), The 5-year survival rate is as low as 20% (Abbas and Krasna, 2017). The mechanism that drives the evolution of EC is still unclear. On this basis, we identified the key genes and molecular pathways that may be related to the progression of esophageal adenocarcinoma and squamous cell carcinoma to find potential markers or therapeutic targets
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