Anticancer Effects of Emodin on HepG2 Cell: Evidence from Bioinformatic Analysis
Autor: | Ying Tang, Zeng Jie Ye, Ruisheng Zhou, Qin-feng Sun, Dai-Han Zhou, Xiong-Wen Wang, Jian-wei Liu |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Carcinoma
Hepatocellular Emodin Article Subject Protein digestion lcsh:Medicine General Biochemistry Genetics and Molecular Biology Receptors G-Protein-Coupled chemistry.chemical_compound Downregulation and upregulation Protein Interaction Mapping Biomarkers Tumor Humans Receptors Somatostatin Receptors Lysophosphatidic Acid Neuropeptide signaling pathway Gene Regulation of gene expression General Immunology and Microbiology Receptors Purinergic P2 Gene Expression Profiling lcsh:R Liver Neoplasms Computational Biology General Medicine Hep G2 Cells Lipopolysaccharide binding Gene expression profiling Gene Expression Regulation Neoplastic chemistry Cancer research Transcriptome Software Research Article Signal Transduction |
Zdroj: | BioMed Research International BioMed Research International, Vol 2019 (2019) |
ISSN: | 2314-6141 2314-6133 |
Popis: | Hepatocellular carcinoma (HCC) is a primary cause of cancer-related death in the world. Despite the fact that there are many methods to treat HCC, the 5-year survival rate of HCC is still at a low level. Emodin can inhibit the growth of HCC cells invitroand invivo. However, the gene regulation of emodin in HCC has not been well studied. In our research, RNA sequencing technology was used to identify the differentially expressed genes (DEGs) in HepG2 cells induced by emodin. A total of 859 DEGs were identified, including 712 downregulated genes and 147 upregulated genes in HepG2 cells treated with emodin. We used DAVID for function and pathway enrichment analysis. The protein-protein interaction (PPI) network was constructed using STRING, and Cytoscape was used for module analysis. The enriched functions and pathways of the DEGs include positive regulation of apoptotic process, structural molecule activity and lipopolysaccharide binding, protein digestion and absorption, ECM-receptor interaction, complement and coagulation cascades, and MAPK signaling pathway. 25 hub genes were identified and pathway analysis revealed that these genes were mainly enriched in neuropeptide signaling pathway, inflammatory response, and positive regulation of cytosolic calcium ion concentration. Survival analysis showed that LPAR6, C5, SSTR5, GPR68, and P2RY4 may be involved in the molecular mechanisms of emodin therapy for HCC. A quantitative real-time PCR (qRT-PCR) assay showed that the mRNA levels of LPAR6, C5, SSTR5, GPR68, and P2RY4 were significantly decreased in HepG2 cells treated with emodin. In conclusion, the identified DEGs and hub genes in the present study provide new clues for further researches on the molecular mechanisms of emodin. |
Databáze: | OpenAIRE |
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