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Molecular Network Profiling in Intestinal- and Diffuse-Type Gastric Cancer

Epithelial-mesenchymal transition (EMT) plays an important role in the acquisition of cancer stem cell (CSC) feature and drug resistance, which are the main hallmarks of cancer malignancy. Although previous findings have shown that several signaling pathways are activated in cancer progression, the...

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Bibliographic Details
Published in:Cancers 2020-12, Vol.12 (12), p.3833
Main Authors: Tanabe, Shihori, Quader, Sabina, Ono, Ryuichi, Cabral, Horacio, Aoyagi, Kazuhiko, Hirose, Akihiko, Yokozaki, Hiroshi, Sasaki, Hiroki
Format: Article
Language:English
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Summary:Epithelial-mesenchymal transition (EMT) plays an important role in the acquisition of cancer stem cell (CSC) feature and drug resistance, which are the main hallmarks of cancer malignancy. Although previous findings have shown that several signaling pathways are activated in cancer progression, the precise mechanism of signaling pathways in EMT and CSCs are not fully understood. In this study, we focused on the intestinal and diffuse-type gastric cancer (GC) and analyzed the gene expression of public RNAseq data to understand the molecular pathway regulation in different subtypes of gastric cancer. Network pathway analysis was performed by Ingenuity Pathway Analysis (IPA). A total of 2815 probe set IDs were significantly different between intestinal- and diffuse-type GC data in cBioPortal Cancer Genomics. Our analysis uncovered 10 genes including ( ), ( ), ( ), ( ), ( ), ( ), ( ), ( ), ( ), and ( ), which have differences in gene expression between intestinal- and diffuse-type GC. A total of 463 direct relationships with three molecules (MYC, NTRK1, UBE2M) were found in the biomarker-filtered network generated by network pathway analysis. The networks and features in intestinal- and diffuse-type GC have been investigated and profiled in bioinformatics. Our results revealed the signaling pathway networks in intestinal- and diffuse-type GC, bringing new light for the elucidation of drug resistance mechanisms in CSCs.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers12123833