Abstract
BackgroundPancreatic cancer is a common malignant tumor of the digestive tract. It has a high degree of malignancy and poor prognosis. Finding effective molecular markers has great significance for pancreatic cancer diagnosis and treatment. This study aimed to investigate DLGAP5 expression in pancreatic cancer and explore the possible mechanisms and clinical value of DLGAP5 in tumorigenesis and tumor development.MethodsDifferentially expressed genes were screened using the Gene Expression Omnibus (GEO) data set GSE16515. Gene Ontology (GO)-based functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis were performed on the corresponding proteins of the above genes using the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The Kaplan–Meier Plotter database was used to analyze the relationship between differentially expressed genes and pancreatic cancer prognosis. The most prognostic gene, DLGAP5, was screened out, and the Oncomine and gene expression profiling interactive analysis (GEPIA) databases were used to analyze its expression in pancreatic cancer and other cancer tissues. The Cancer Genome Atlas (TCGA) database was used to analyze the overall survival of DLGAP5. Gene set enrichment analysis (GSEA) was performed to explore its possible molecular mechanisms in pancreatic cancer. Furthermore, the biological behavior of DLGAP5 in pancreatic cancer was verified by cell function experiments.ResultsA total of 201 significant upregulated differentially expressed genes and 79 downregulated genes were selected. The biological processes with significant enrichment of differential genes included cell adhesion, apoptosis, wound healing, leukocyte migration, angiogenesis. Pathways were mainly enriched in tumor-related signaling pathways such as cancer pathways, the extracellular matrix-receptor interaction pathway, and the p53 signaling pathway. DLGAP5 was significantly expressed in pancreatic cancer, and its expression level had a significant effect on patients’ survival time and progression-free survival. GSEA results indicated that DLGAP5 had significantly enriched into signaling pathways such as the cell cycle, the p53 signaling pathway, and oocyte meiosis. The experimental results showed that when we knocked down the expression of DLGAP5 in pancreatic cancer cells, their proliferation ability was significantly inhibited, and their invasion and migration ability significantly decreased.ConclusionsDLGAP5 can be used as a prognostic indicator for pancreatic cancer and affect the occurrence and development of pancreatic cancer.
Highlights
Pancreatic cancer is a common malignant tumor of the digestive tract that is characterized by insidious onset, a high degree of malignancy, and rapid development [1]
Bioinformatics analysis Selecting differential genes from the Gene Expression Omnibus (GEO) database The pancreatic cancer data set GSE16515 was obtained from the GEO
Construction of the protein interaction network The structure of the differentially expressed genes’ protein interaction network is shown in Fig. 2a, which contained 15 nodes and 97 edges. It was obtained from the Differentially expressed genes (DEGs) protein– protein interaction (PPI) network using Molecular Complex Detection (MCODE) (Fig. 2b)
Summary
Pancreatic cancer is a common malignant tumor of the digestive tract. It has a high degree of malig‐ nancy and poor prognosis. Finding effective molecular markers has great significance for pancreatic cancer diagnosis and treatment. Pancreatic cancer is a common malignant tumor of the digestive tract that is characterized by insidious onset, a high degree of malignancy, and rapid development [1]. Pancreatic cancer prognosis is poor, with a 5-year survival rate of 8% [4]. A number of research studies have shown that genes play vital roles in the incidence and development of pancreatic cancer [7,8,9,10,11]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call