Objective: To evaluate the effect of hypoxia on migration, invasion and adhesion to endothelium of human pulmonary adenocarcinoma A549 cells. Methods: Wound-healing and Transwell invasion assays were performed to stud...Objective: To evaluate the effect of hypoxia on migration, invasion and adhesion to endothelium of human pulmonary adenocarcinoma A549 cells. Methods: Wound-healing and Transwell invasion assays were performed to study the effect of hypoxia on migration and invasion of A549 cells, and A549 cells were added to a monolayer of human umbilical vein endothelial cells (HUVECs) to test the ability to adhere to endothelium. Immunofluorescence assay and luciferase reporter gene assay were also used to evaluate the effect of hypoxia on distribution of E-cadherin, β-catenin, and actin, and hypoxia-inducible factor-1 (HIF-1)-dependent transcription, respectively. Results: Hypoxia facilitated A549 cell migration, invasion, and A549 cell-endothelial cells adhesion, and modulated the distribution of E-cadherin and β-catenin, and actin cytoskeleton rearrangement, and up-regulated HIF-1-dependent reporter gene expression in A549 cells. Conclusion: Promotion of A549 cell migration, invasion, and adhesion on endothelium by hypoxia might be modulated through its up-regulating HIF-1-dependent gene expression, which then induced the redistribution of E-cadherin and β-catenin, and the actin cytoskeletal reorganization.展开更多
文摘Objective: To evaluate the effect of hypoxia on migration, invasion and adhesion to endothelium of human pulmonary adenocarcinoma A549 cells. Methods: Wound-healing and Transwell invasion assays were performed to study the effect of hypoxia on migration and invasion of A549 cells, and A549 cells were added to a monolayer of human umbilical vein endothelial cells (HUVECs) to test the ability to adhere to endothelium. Immunofluorescence assay and luciferase reporter gene assay were also used to evaluate the effect of hypoxia on distribution of E-cadherin, β-catenin, and actin, and hypoxia-inducible factor-1 (HIF-1)-dependent transcription, respectively. Results: Hypoxia facilitated A549 cell migration, invasion, and A549 cell-endothelial cells adhesion, and modulated the distribution of E-cadherin and β-catenin, and actin cytoskeleton rearrangement, and up-regulated HIF-1-dependent reporter gene expression in A549 cells. Conclusion: Promotion of A549 cell migration, invasion, and adhesion on endothelium by hypoxia might be modulated through its up-regulating HIF-1-dependent gene expression, which then induced the redistribution of E-cadherin and β-catenin, and the actin cytoskeletal reorganization.
