Down-regulation of CLEC3B facilitates epithelial-mesenchymal transition, migration and invasion of lung adenocarcinoma cells
Copyright policy )Down-regulation of CLEC3B facilitates epithelial-mesenchymal transition, migration and invasion of lung adenocarcinoma cells
Lung adenocarcinoma (LUAD) belongs to non-small cell lung carcinoma, and the metastasis is the main cause of death in LUAD patients. It is generally accepted that cell adhesion is closely associated with tumor metastasis. Accordingly, the purpose of this study is to investigate the functions of CLEC3B to the invasion, adhesion, and migration of LUAD cells.Through bioinformatic analysis, CLEC3B level was found markedly down-regulated in LUAD tissue. Parallel-plate flow chamber, wound-healing and Transwell assays were taken to detect the cell adhesion, invasion, and migration. qRT-PCR and western blot analyzed expression of CLEC3B, p53 and epithelial-mesenchymal transition (EMT) marker.When CLEC3B was lowly-expressed in LUAD cell lines, the cell adhesion capability was also lowered, with the EMT, migration and invasion of the cells progressed. Abnormal expression of CLEC3B was related to p53 signaling pathway.Above all, a further investigation of the function of CLEC3B in LUAD helps us further understand the molecular mechanism of the tumor metastasis.
- Zhejiang Provincial People's Hospital China (People's Republic of)
Epithelial-Mesenchymal Transition, Lung Neoplasms, Down-Regulation, Adenocarcinoma of Lung, Gene Expression Regulation, Neoplastic, Cell Movement, Cell Line, Tumor, Humans, Lectins, C-Type, Tumor Suppressor Protein p53, Cell Proliferation
Epithelial-Mesenchymal Transition, Lung Neoplasms, Down-Regulation, Adenocarcinoma of Lung, Gene Expression Regulation, Neoplastic, Cell Movement, Cell Line, Tumor, Humans, Lectins, C-Type, Tumor Suppressor Protein p53, Cell Proliferation
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