Abstract
Chinese medicines are an important source of secondary metabolites with excellent antitumour activity. Evodia rutaecarpa, from the family Rutaceae, exhibits antitumour activity. Evodiamine (EVO), which was isolated from the fruit of E. rutaecarpa, exhibits robust antitumour activity. However, the antitumour mechanism of EVO remains unclear. In this study, we assessed the growth-inhibiting effect of EVO on two renal carcinoma cell lines. We found that EVO could change the morphology and decrease the viability and proliferation of cells in a time- and concentration-dependent manner in vitro. In addition, transcriptome analysis indicated that EVO can modulate the transcriptome of Caki-1 cells. In total, 7,243 differentially expressed genes were found, among which 3,347 downregulated genes and 3,896 upregulated genes were mainly involved in cell migration, apoptosis, cell cycle, and DNA replication. Furthermore, we demonstrated that EVO can cause apoptosis, arrest cells in the G2/M phase, and regulate the expression of apoptosis- and cell cycle-related genes in Caki-1 cells. Our study reveals the anticancer effects of EVO using cellular and molecular data, and indicates the potential uses of this compound as a resource to characterize the antitumour mechanisms of E. rutaecarpa.
Highlights
Disruption of the mitochondrial membrane potential, resulting from JNK- and PERK-mediated phosphorylation of the Bcl-2 protein[22]
We investigated the inhibitory activity of EVO against the proliferation of three cell lines (human renal carcinoma cell lines (786-O and Caki-1 cells), and the human renal epithelial cell line HK-2) using the Cell Counting Kit-8 (CCK-8) assay
We found that EVO decreased the viability of these three cell lines in a time- and concentration-dependent manner (Fig. 1a,b)
Summary
Disruption of the mitochondrial membrane potential, resulting from JNK- and PERK-mediated phosphorylation of the Bcl-2 protein[22]. The mechanism by which EVO exerts its anticancer effects on renal carcinoma cells requires further research. Cytological experiments and a transcriptome profiling study were performed to reveal the anticancer mechanism of EVO. A series of experiments investigating the viability and proliferation of human renal carcinoma 786-O cells and Caki-1 cells and the human renal epithelial cell line HK-2 was performed under EVO treatment. A transcriptome profiling study was used to analyse EVO-regulated genes and signalling pathways responsible for growth and apoptosis using RNA sequencing. We verified the molecular mechanisms through which EVO inhibits growth and induces apoptosis using ultrastructural observations, flow cytometry analysis, and qPCR
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