J Cancer 2019; 10(13):2849-2856. doi:10.7150/jca.31338 This issue
1. School of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, 210023, P.R. China
2. Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine (TCM) Prevention and Treatment of Tumor, Nanjing University of Chinese Medicine, Nanjing, 210023, P.R. China
*Cheng Hu and Rilei Jiang contributed equally to this article.
Ophiopogonin-B (OP-B) has been reported to suppress metastasis and angiogenesis of adenocarcinoma A549 cells in vitro and in vivo. More and more evidences indicate that inflammatory microenvironment facilitates tumor metastasis. Digital Gene Expression (DGE) analysis of non-small cell lung cancer (NSCLC) cell lines showed that OP-B downregulated the expression of linc00668, which promoted progression of cancer. Herein, we simulated the inflammatory microenvironment by co-culturing A549 cells with LPS-treated THP-1 cells and found that the level of linc00668 increased significantly in the mock group, while OP-B treatment inhibited the level of linc00668 and reversed epithelial-mesenchymal transition (EMT) induced by linc00668. In addition, overexpression of linc00668 in A549 cells suppressed the expression of E-cadherin and induced expression of N-cadherin, while OP-B treatment reversed these changes. Bioinformatic prediction and dual-luciferase reporter gene assay validated that linc00668 sponge miR-432-5p and at last acted on EMT to execute the anti-migration function of A549 cells under inflammatory microenvironment. Taken together, OP-B inhibits metastasis of A549 cells via the linc00668/miR-432-5p/EMT axis.
Keywords: NSCLC, metastasis, linc00668, miR-432-5p, epithelial-mesenchymal transition (EMT)