Identification of genes in hepatocellular carcinoma induced by non-alcoholic fatty liver disease

Autor: Chaohui Yu, Xin Song, Changzhou Cai
Rok vydání: 2020
Předmět:
Male
Cancer Research
Carcinoma
Hepatocellular
Chromosomal Proteins
Non-Histone
RHOB
Expression
Biology
03 medical and health sciences
0302 clinical medicine
Non-alcoholic Fatty Liver Disease
Extracellular exosome
CDC2 Protein Kinase
Gene expression
Biomarkers
Tumor
Genetics
medicine
Humans
Gene Regulatory Networks
HSP90 Heat-Shock Proteins
Protein Interaction Maps
rhoB GTP-Binding Protein
Gene
030304 developmental biology
0303 health sciences
Liver Neoplasms
Fatty liver
Computational Biology
Nuclear Proteins
bioinformatics
hepatocellular carcinoma
General Medicine
Cell cycle
Microarray Analysis
medicine.disease
digestive system diseases
Gene Expression Regulation
Neoplastic
Protein Kinase C-delta
PRKCD
Oncology
030220 oncology & carcinogenesis
Hepatocellular carcinoma
Mad2 Proteins
Disease Progression
Cancer research
CEP192
Female
Research Article
Zdroj: Cancer Biomarkers
ISSN: 1875-8592
1574-0153
DOI: 10.3233/cbm-190169
Popis: BACKGROUND: Hepatocellular carcinoma (HCC) is the leading cause of mortality worldwide. In recent years, the incidence of HCC induced by NAFLD is growing rapidly. OBJECTIVE: To screen for new pathogenic genes and related pathways both in NAFLD and HCC, and to explore the pathogenesis of progression from NAFLD to HCC. METHODS: Gene expression microarrays (GSE74656, GSE62232) were used for identifying differentially expressed genes (DEGs). Functional enrichment and pathway enrichment analyses indicated that these DEGs were related to cell cycle and extracellular exosome, which were closely related to NAFLD and HCC development. We then used the Search Tool for the Retrieval of Interacting Genes (STRING) to establish the protein-protein interaction (PPI) network and visualized them in Cytoscape. And the overall survival (OS) analysis and gene expression validation in TCGA of hub genes was performed. RESULTS: Seven hub genes, including CDK1, HSP90AA1, MAD2L1, PRKCD, ITGB3BP, CEP192, and RHOB were identified. Finally, we verified the expression level of ITGB3BP and CEP192 by quantitative real-time PCR in vitro. CONCLUSIONS: The present study implied possible DEGs, especially the new gene CEP192, in the progression of NAFLD developing to HCC. Further rigorous experiments are required to verify the above results.
Databáze: OpenAIRE
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