[Effect of transcriptional factor snail on epithelial-mesenchymal transition and tumor metastasis].
Ali Zhang, Quansheng Wang, Yahua Zhong, Gang Chen, Ling Xi, Conghua Xie, Yunfeng Zhou, Ding Ma
Abstract
Ali Zhang, Quansheng Wang, Yahua Zhong, Gang Chen, Ling Xi, Conghua Xie, Yunfeng Zhou, Ding Ma
Abstract
BACKGROUND & OBJECTIVE: Transcription factor Snail mediates epithelial-mesenchymal transition (EMT), and is associated with tumor metastasis. This study was designed to observe the enhancive effect of Snail and the reverse effect of antisense-Snail on EMT of tumor cells, and explore the role of Snail in tumor metastasis. METHODS: Snail cDNA was transfected into canine renal epithelial cell line MDCK; antisense-Snail was transfected into human breast cancer cell line MDA-MB231. The expression of epithelial markers E-cadherin, beta-catenin and Cytokeratin 18, mesenchymal marker Fibronectin, metastasis-related marker matrix metalloproteinase-2 (MMP-2), and RhoA were detected by Western blot. The metastatic potential of tumor cells was examined by in vitro cell wound model and Boyden chamber invasion assay. RESULTS: The invasion potential of MDCK cells was enhanced after transfection of Snail. The expression of E-cadherin, beta-catenin, and Cytokeratin 18 was significantly lower in Snail-transfected MDCK cells than in control cells (P < 0.05); the expression of Fibronectin, MMP-2, and RhoA was significantly higher in Snail-transfected cells than in control cells (P < 0.05). Inhibiting the expression of Snail with antisense-Snail in MDA-MB231 cells led to opposite results. CONCLUSION: Snail promotes EMT in normal epithelial cells, and inhibiting the expression of Snail may reverse EMT and suppress tumor metastasis.
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BACKGROUND & OBJECTIVE: Transcription factor Snail mediates epithelial-mesenchymal transition (EMT), and is associated with tumor metastasis. This study was designed to observe the enhancive effect of Snail and the reverse effect of antisense-Snail on EMT of tumor cells, and explore the role of Snail in tumor metastasis. METHODS: Snail cDNA was transfected into canine renal epithelial cell line MDCK; antisense-Snail was transfected into human breast cancer cell line MDA-MB231. The expression of epithelial markers E-cadherin, beta-catenin and Cytokeratin 18, mesenchymal marker Fibronectin, metastasis-related marker matrix metalloproteinase-2 (MMP-2), and RhoA were detected by Western blot. The metastatic potential of tumor cells was examined by in vitro cell wound model and Boyden chamber invasion assay. RESULTS: The invasion potential of MDCK cells was enhanced after transfection of Snail. The expression of E-cadherin, beta-catenin, and Cytokeratin 18 was significantly lower in Snail-transfected MDCK cells than in control cells (P < 0.05); the expression of Fibronectin, MMP-2, and RhoA was significantly higher in Snail-transfected cells than in control cells (P < 0.05). Inhibiting the expression of Snail with antisense-Snail in MDA-MB231 cells led to opposite results. CONCLUSION: Snail promotes EMT in normal epithelial cells, and inhibiting the expression of Snail may reverse EMT and suppress tumor metastasis.
Key concepts: Snail, Epithelial–mesenchymal transition, Biology, RHOA, Transfection, Metastasis, Vimentin, Cancer research