GENE - GENE INTERACTION INTERACTOME OF PERIODONTAL DISEASE AND PANCREATIC CANCER LEAD BY ANGIOGENESIS PATHWAY AND EPIDERMAL GROWTH FACTOR RECEPTOR SIGNALING PATHWAY.

Autor: DHIVYADHARSHINI, J., RAJASEKAR, Arvina
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Zdroj: International Journal of Medical Dentistry; Apr-Jun2023, Vol. 27 Issue 2, p189-195, 7p
Abstrakt: Introduction: The polypeptide molecule epidermal growth factor (EGF) is a multifactorial cytokine acting in cell growth, proliferation, and wound healing. Parkinson's disease, a number of cancers and inflammatory disorders have all been reported as correlated with serum EGF levels. Therefore, this study aims at investigating the association between pancreatic cancer and periodontitis via EGF and angiogenesis pathways. Materials and methods: Differentially expressed genes (DEGs) of periodontitis and pancreatic cancer were identified from the datasets retrieved from the Gene Expression Omnibus database. GeneMANIA was used to visualize the molecular interaction networks. By ranking the scores of each node of molecular interaction, important nodes of protein interactions were obtained. The hub genes were ranked and those with a degree = 20 were selected. A network of genes and their co-expression genes were analyzed. Gene ontology of the corresponding genes was also assessed. Results and discussion: There is a significant correlation between periodontitis and pancreatic cancer. The most significant biological process for upregulated genes involves angiogenesis, EGF receptor signaling pathway, cytokine mediated signaling pathway and chemokine signaling pathway. Molecular function enrichment assessment for most significant upregulated genes included chemokine receptor binding, catalytic activity, molecular function regulator, molecular transducer activity and transcription regulator activity. The top five ranked hub genes involved in the interactome are SLF2, PECAM1, LIFR, ESYT2 and GSDMC. Conclusions: A positive gene to gene interaction interactome between periodontal disease and pancreatic cancer was observed. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index