β-elemene suppresses the epithelial-mesenchymal transition of non-small-cell lung cancer via the wnt/β-catenin pathway

Objective: Lung cancer is the leading cause of cancer-associated deaths worldwide. Of the various types of lung cancer, non-small-cell lung cancer (NSCLC) has the highest incidence. The epithelial-to-mesenchymal transition (EMT) in the tumor microenvironment plays an significant role in NSCLC invasion and tumor metastasis. The Wnt/beta-catenin pathway has been shown to involve the EMT in NSCLC. In our study, we profiled beta-elemene expression and its related functions on the proliferation, apoptosis, invasion, and EMT in two different types of NSCLC cells. Method: During this study, we used A549 and H1299 cells. The cell proliferation was assessed with the MTT experiments. The apoptotic cell death was assessed using an Annexin V/PI detection kit. The cell invasion ability was assessed through Transwell assays. The Wnt/beta-catenin pathway target gene expression and the related EMT protein was determined through Western blotting. Results: We demonstrated that beta-elemene downregulates the A549 and H1299 proliferation abilities and induces cell apoptosis in a concentration-based way. We found that the pretreatment of cells with beta-elemene for 24 h decreases invasion. We also demonstrated that beta-elemene upregulates the level of the EMT-related protein E-cadherin and downregulates the vimentin, beta-catenin, and N-cadherin levels. The triggering of Wnt/beta-catenin signaling by LiCl reverses the influence of beta-elemene on NSCLC cell invasion and the expression of the EMT-related transcription factors. In addition, LiCl also reverses the influence of beta-elemene on NSCLC cell proliferation and the apoptotic process. Conclusion: Our findings show that beta-elemene suppresses the EMT and the invasion of NSCLC cells via the Wnt/beta-catenin pathway for the first time, suggesting that beta-elemene may prevent NSCLC metastasis.