Abstract
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 in vitro and in vivo. 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.
Highlights
Hepatocellular carcinoma (HCC) is a severe disease of the digestive system and is the sixth most common and second leading cause of death due to cancer
Treatment of HepG2 cells via emodin dose-response assays revealed that emodin had IC50 values of about 20 μM at 72 h
The whole transcriptomic profiles of HepG2 cells and of those treated with emodin were assessed at base-pair resolution via RNA sequencing
Summary
Hepatocellular carcinoma (HCC) is a severe disease of the digestive system and is the sixth most common and second leading cause of death due to cancer. Regorafenib, and lenvatinib, as well as immunotherapy with a PD-1 inhibitor (nivolumab), have been approved for the treatment of advanced-stage HCC [4,5,6,7]. There remains an urgent need for the identification and development of novel therapeutic agents and strategies for the treatment of HCC. Emodin (1,3,8-trihydroxy-6-methylanthraquinone; Figure 1) is an active ingredient derived from Polygonum cuspidatum [8], Rheum palmatum [9], Cassia occidentalis [10], and Polygonum multiflorum [11] and has been used in China for many centuries. Modern pharmacological studies have revealed that emodin exhibits various biological activities, such as apoptosis-inducing and antiproliferative
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