Ophiopogonin-B (OP-B) has been reported to suppress metastasis and angiogenesis of adenocarcinoma A549 cells and . 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 linc... More
Ophiopogonin-B (OP-B) has been reported to suppress metastasis and angiogenesis of adenocarcinoma A549 cells and . 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.
