Emodin treatment of HepG2 cells resulted in 859 differentially expressed genes, significantly decreasing mRNA levels of LPAR6, C5, SSTR5, GPR68, and P2RY4, suggesting potential anticancer mechanisms.
. 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.
Zhou et al. (Sun,) conducted a other in Hepatocellular carcinoma (HepG2 cells). Emodin was evaluated on Differentially expressed genes (DEGs). Emodin treatment of HepG2 cells resulted in 859 differentially expressed genes, significantly decreasing mRNA levels of LPAR6, C5, SSTR5, GPR68, and P2RY4, suggesting potential anticancer mechanisms.