Y Li1, X-B Guo, Y-H Wei. 1. Department of Pathology, The Affiliated Hexian Memorial Hospital of Southern Medical University, Guangzhou, P.R. China. raywei198011@163.com.
Abstract
OBJECTIVE: To study the mechanism of lncRNA GAS5 affecting epithelial-mesenchymal transition and invasion of breast cancer cells by regulating miR-216b. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expressions of GAS5 and miR-216b in breast cancer and paracancerous tissues. The relationship between GAS5 and clinicopathological parameters of breast cancer patients was analyzed. The Dual-Luciferase reporter gene was used to detect the interaction between GAS5 and miR-216b and the transwell invasion assay was used to detect the invasive ability of lung cancer cells after GAS5 inhibition. Apoptosis assay was used to detect the apoptosis of breast cancer cells after GAS5 inhibition. Western blotting and immunofluorescence staining were used to detect the inhibition of GAS5 epithelial-mesenchymal transition. RESULTS: Compared with paracancerous tissues, in breast cancer tissues, the expression of GAS5 was increased and the expression of miR-216b was decreased. As the patients enter the later stages of breast cancer, the expression level of GAS5 in breast cancer patients was significantly elevated. The expression of GAS5 in the tissues with lymph node metastasis of breast cancer was markedly increased. The inhibition of GAS5 can promote the apoptosis of breast cancer cells; GAS5 can specifically bind to the 3' UTR of miR-216b. The expression of GAS5 inhibited the expression of E-cadherin in breast cancer cells and significantly upregulated N-cadherin, which has been confirmed by immunofluorescence staining experiments. CONCLUSIONS: GAS5 plays an important role in the development of breast cancer. GAS5 can target on miR-216b to regulate the biological behavior and epithelial-mesenchymal transition of breast cancer cells.
OBJECTIVE: To study the mechanism of lncRNA GAS5 affecting epithelial-mesenchymal transition and invasion of breast cancer cells by regulating miR-216b. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expressions of GAS5 and miR-216b in breast cancer and paracancerous tissues. The relationship between GAS5 and clinicopathological parameters of breast cancerpatients was analyzed. The Dual-Luciferase reporter gene was used to detect the interaction between GAS5 and miR-216b and the transwell invasion assay was used to detect the invasive ability of lung cancer cells after GAS5 inhibition. Apoptosis assay was used to detect the apoptosis of breast cancer cells after GAS5 inhibition. Western blotting and immunofluorescence staining were used to detect the inhibition of GAS5 epithelial-mesenchymal transition. RESULTS: Compared with paracancerous tissues, in breast cancer tissues, the expression of GAS5 was increased and the expression of miR-216b was decreased. As the patients enter the later stages of breast cancer, the expression level of GAS5 in breast cancerpatients was significantly elevated. The expression of GAS5 in the tissues with lymph node metastasis of breast cancer was markedly increased. The inhibition of GAS5 can promote the apoptosis of breast cancer cells; GAS5 can specifically bind to the 3' UTR of miR-216b. The expression of GAS5 inhibited the expression of E-cadherin in breast cancer cells and significantly upregulated N-cadherin, which has been confirmed by immunofluorescence staining experiments. CONCLUSIONS:GAS5 plays an important role in the development of breast cancer. GAS5 can target on miR-216b to regulate the biological behavior and epithelial-mesenchymal transition of breast cancer cells.