Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a malignant tumor with a high degree of malignancy that is difficult to diagnose and treat. The present study integrated PDAC cohort profile datasets to identify key candidate genes and pathways involved in the pathogenesis of the disease. The expression profiles of GSE28735 included 45 PDCA and matching pairs of adjacent non-tumor tissue. Differentially expressed genes (DEGs) were sorted and candidate genes and pathway enrichment were analyzed. A DEG-associated protein-protein interaction (PPI) network was constructed. A total of 424 DEGs were identified in PDAC, including 159 upregulated genes and 265 downregulated genes. Gene Ontology analysis results indicated that upregulated DEGs were significantly enriched in biological process, molecular function and cellular component categories. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that the upregulated DEGs were enriched in ‘pancreatic secretion’, ‘protein digestion’ and ‘absorption’. Downregulated DEGs were enriched in ‘ECM-receptor interaction’, ‘focal adhesion’ and ‘PI3K/AKT’ signaling pathways. The PPI network revealed that these genes were involved in significant pathways, including ‘ECM organization’ signaling pathways (Hippo signaling pathway, TGF-β signaling pathway, Hedgehog signaling pathway and Wnt signaling pathway), ‘serine-type peptidase activity’ signaling pathway (PI3K-Akt signaling pathway, TNF-α signaling pathway and Wnt signaling pathway) and ‘extracellular region’ signaling pathways (RTP signaling pathway, G protein-coupled receptor signaling pathway and RAS-RAF-MAPK signaling pathway). The identification of these candidate genes and pathways sheds light on the etiology and molecular mechanisms of PDAC and may guide the development of novel therapies for pancreatic cancer.
Highlights
Pancreatic cancer has a poor prognosis, with a median survival time of 3‐6 month and a 5‐year survival rate of less than 5% [1,2,3]
Numerous studies have focused on the pathogenesis and progression of pancreatic cancer, the etiology and molecular mechanisms of pancreatic cancer remain unclear [5,6]
For cellular component (CC), the upregulated Differentially expressed genes (DEGs) were enriched in the ‘extracellular region’, and the downregulated DEGs were enriched in ‘extracellular region’ and ‘ECM’ (Tables II and III)
Summary
Pancreatic cancer has a poor prognosis, with a median survival time of 3‐6 month and a 5‐year survival rate of less than 5% [1,2,3]. Numerous studies have focused on the pathogenesis and progression of pancreatic cancer, the etiology and molecular mechanisms of pancreatic cancer remain unclear [5,6]. Previous scientific studies have demonstrated that the occurrence and progression of pancreatic cancer involve the interaction of several factors, including gene mutations and environmental conditions [7,8]. There remains a lack of information regarding the molecular mechanisms that cause the development and progression of pancreatic cancer that would allow for improved precision therapies. Understanding the molecular mechanisms of pancreatic cancer can provide an effective basis for early prevention, diagnosis and treatment
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