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AIM: To explore the effect of N-cadherin knock-down on the biological behavior of EC9706 cells in vivo.METHODS: The control vector pEGFP-MSCVneo and recombinant retroviral vector pMSCVneo/N-cadherin plasmids were transfected into esophageal squamous cell carcinoma(ESCC) cell line EC9706 according to the manufacturer's instructions. Stable EC9706 cell clones were selected using selection medium containing G418. Untreated EC9706 cells, control vector-transfected EC9706 cells and N-cadherin RNAi-transfected EC9706 cells were inoculated subcutaneously into the right flank of BALB/c mice (5 for each group), respectively. When tumors became palpable, the diameters of the tumors were measured with a caliper each week after subcutaneous implantation, and the volume (mm3) and weight (g) of the tumors were also calculated. Immunohistochemistry and Western blotting were employed to examine the expression levels of E-cadherin, N-cadherin and MMP-9 in the tumor tissues. The cell apoptosis was analyzed by TUNEL method.RESULTS: Compared with untreated group and control vector group, there was an obvious decrease in the volumes and weights of the tumors in N-cadherin RNAi group (P<0.05). No difference of E-cadherin expression in the 3 groups was observed. However, the expression of N-cadherin and MMP-9 in N-cadherin RNAi group was apparently reduced, and the positive number of cell apoptosis was obviously increased in N-cadherin RNAi group (106.81±6.47) as compared with that in untreated group (51.55±4.68) and control vector group (54.17±5.26). CONCLUSION: N-cadherin knock-down inhibits the tumor formation of EC9706 cells in nude mice by decreasing MMP-9 expression, resulting in less degradation of ECM and less aggression of the cancer cells. N-cadherin is an important factor in the progression and metastasis of ESCC,and may serve as a potential molecular target for biotherapy of ESCC.  相似文献   
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Myogenesis, the formation of muscle fibers, is affected by certain glycoproteins, including chondroitin sulfate (CS), which are involved in various cellular processes. We aimed to investigate the mechanism underlying CS-E-induced suppression of myotube formation using the myoblast cell line C2C12. Differentiated cells treated with 0.1 mg/ml CS-E for nine days showed multinucleated and rounded myotubes with myosin heavy chain positivity. No difference was found between the CS-E-treated group with rounded myotubes and CS (−) controls with elongated myotubes in the levels of phospho-cofilin, a protein involved in the dynamics of actin cytoskeleton. Interestingly, N-cadherin, which is involved in the gene expression of myoblast fusion factors (myomaker and myomixer), was significantly downregulated at both the mRNA and protein levels following CS-E treatment. These results suggest that N-cadherin downregulation is one of the mechanisms underlying the CS-E-induced suppression of myotube formation.  相似文献   
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AIM: To investigate the role of N-cadherin in the delamination of neural crest cells. METHODS: The normal expression of N-cadherin in neural tube was identified using in situ hybridization. The cells with N-cadherin over expression were obtained by transfection of wild-type N-cadherin (wt-N-cadherin),and the cells with N-cadherin silencing expression were obtained by transfection of dominant-negative N-cadherin (dn-N-cadherin). The migration of cranial neural crest cells was determined by the technique of immunohistochemistry. RESULTS: Either overexpression or down-regulation of N-cadherin significantly affected the migration of cranial neural crest cells. CONCLUSION: Delamination and migration of the cranial neural crest cells rely on the relative N-cadherin expression in the neural tube during neurulation.  相似文献   
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