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Published on: November 5, 2020
Identification of molecular mechanisms of glutamine in pancreatic cancer
Zhen-Yi Jia1, Tong-Yi Shen1, Wei Jiang2
1Department of Gastrointestinal Surgery, Shanghai Tenth People's Hospital Affiliated to Tongji University, Shanghai 200072, P.R. China.
Abstract:
The aim of the present study was to explore the critical genes and molecular mechanisms in pancreatic cancer (PC) cells with glutamine. By analyzing microarray data GSE17632 from the Gene Expression Omnibus database, the DEGs between PC cells treated with glutamine and without glutamine were evaluated. Additionally, function enrichment analyses and protein-protein interaction (PPI) network construction of DEGs were performed. Network module and literature mining analyses were performed to analyze the critical DEGs in PC cells. In total, 495 genes were selected as DEGs between control and glutamine cells in PC. These DEGs were mainly enriched in several Gene Ontology (GO) terms in biological process, cellular components and molecular function. Additionally, they were also enriched in certain pathways, including metabolic pathways and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. MYC, heat shock 70kDa protein 5 (HSPA5), interleukin 8 (IL8), and chemokine (C-X-C motif) receptor 4 (CXCR4) were hub genes in the PPI network. Furthermore, two sub-network modules of PPI network and two co-occurrence networks were obtained. The DEGs of MYC, HSPA5, IL18 and CXCR4 may exert important roles in molecular mechanisms of PC cells with glutamine.
Insights
This study identifies key genes and pathways affected by glutamine in pancreatic cancer (PC) cells. MYC, HSPA5, IL8, and CXCR4 are highlighted as critical genes influencing PC progression.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Pancreatic cancer (PC) is a deadly malignancy with complex molecular underpinnings.
- Glutamine metabolism plays a crucial role in cancer cell proliferation and survival.
- Understanding glutamine's impact on PC molecular mechanisms is vital for therapeutic development.
Purpose of the Study:
- To identify critical genes and molecular mechanisms in pancreatic cancer cells influenced by glutamine.
- To analyze differentially expressed genes (DEGs) and their functional enrichment.
- To construct and analyze protein-protein interaction (PPI) networks for key regulatory genes.
Main Methods:
- Analysis of microarray data (GSE17632) from the Gene Expression Omnibus database.
- Identification of DEGs between glutamine-treated and untreated PC cells.
- Gene Ontology (GO) and pathway enrichment analyses.
- Construction and analysis of PPI networks, including module and literature mining.
Main Results:
- Identified 495 DEGs between control and glutamine-treated PC cells.
- DEGs were enriched in biological processes, cellular components, molecular functions, metabolic pathways, and the JAK-STAT signaling pathway.
- MYC, HSPA5, IL8, and CXCR4 emerged as hub genes in the PPI network.
Conclusions:
- Glutamine significantly alters gene expression in pancreatic cancer cells.
- Key genes including MYC, HSPA5, IL8, and CXCR4 are implicated in the molecular mechanisms of PC under glutamine influence.
- These findings provide insights into glutamine's role in PC pathogenesis and potential therapeutic targets.
