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Effects of tumor suppressor NDRG2 gene on proliferation and invasive ability of colon cancer cell line SW620 / 国际肿瘤学杂志
Article em Zh | WPRIM | ID: wpr-493154
Biblioteca responsável: WPRO
ABSTRACT
Objective To observe the influence of N-myc downstream-regulated gene 2 (NDRG2) on the growth and invasive ability of human colon cancer cell line SW620,and to explore its mechanism.Methods pcDNA3.1-NDRG2 and siRNA-NDRG2 were transfected transiently respectively into SW620 by Lipofectamine TM 2000,untreated cells as the control group.Western blotting was used to investigate the expression of NDRG2 and matrix metalloproteinase-2 (MMP-2).Matrigel invasion assay was used to study the invasive abilities of SW620 cells in all groups.The growth curve was determined through 3-(4,5-dimethyl-2-thiazoly)-2,5-diphenyl-2H-tetrazolium bromide method.Result After transfecting pcDNA3.1-NDRG2 into the SW620 cells,the protein level of NDRG2 increased and the expression of MMP-2 declined markedly.After transfecting siRNA-NDRG2 into the SW620 cells,the protein level of NDRG2 declined and the expression of MMP-2 increased markedly.In addition,compared with the control group (75.80 ± 4.82),the numbers of transmembrane cells in pcDNA3.1 group (56.20 ± 7.40) and in siRNA group (94.20 ± 9.23) were significantly different (t =13.102,P =0.000;t =11.820,P =0.000).The growth curve showed that:compared with the control group (0.67 ±0.01),the absorbance of the fifth day after transfection in pcDNA3.1 group (0.46 ±0.01) and in siRNA group (0.91 ± 0.02) were different significantly (t =9.561,P =0.000;t =10.922,P =0.000).Conclusion NDRG2 can reduce the invasion and proliferation ability of colon cancer cell SW620,and its mechanism may be related to the down-regulation of MMP-2 expression.
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Texto completo: 1 Base de dados: WPRIM Idioma: Zh Revista: Journal of International Oncology Ano de publicação: 2016 Tipo de documento: Article
Texto completo: 1 Base de dados: WPRIM Idioma: Zh Revista: Journal of International Oncology Ano de publicação: 2016 Tipo de documento: Article