Overexpression of Dickkopf-3 induces apoptosis through mitochondrial pathway in human colon cancer
Overexpression of Dickkopf-3 induces apoptosis through mitochondrial pathway in human colon cancer作者机构:Department of GastroenterologyRenmin Hospital of Wuhan UniversityWuhan 430060Hubei ProvinceChina
出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))
年 卷 期:2012年第18卷第14期
页 面:1590-1601页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种]
基 金:Supported by The Fundamental Research Funds for the Central Universities of China No.20103020101000197
主 题:Dickkopf-3 Overexpression Invasion Apotosis Colon cancer Mitochondria
摘 要:AIM:To investigate the mechanisms of the biological roles of Dickkopf-3(Dkk-3) in cell invasion,survival and apoptosis in colon cancer ***:Three human colon cancer cell lines,i.e.,HT-29,LoVo and SW480,were *** of Dkk-3 induced by pEGFP-N1-Dkk-3-GFP plasmid in LoVo cells was performed using Lipofectamine 2000 *** transcription polymerase chain reaction and Western blotting were performed to determine the mRNA and protein expression levels of Dkk-3,*** proliferation assay,cell cycle analysis,hoechst 33258 assay and Matrigel invasion assay were performed on Dkk-3 overexpressing ***:The mRNA and protein expressions of Dkk-3 in HT-29(mRNA:0.06 ± 0.02,protein:0.06 ± 0.01) and LoVo(mRNA:0.07 ± 0.02,protein:0.07 ± 0.02) cells were significantly lower than that in SW480 cells(mRNA:0.92 ± 0.04,protein:0.69 ± 0.13;all P 0.05),and the greatest levels of invasiveness wasin LoVo ***-3 overexpression inhibited the proliferation and invasion of LoVo cells and induced cell cycle arrest at G0/G1 phase and subsequent apoptosis,as indicated by increased chromatin condensation and fragments,upregulated Bax and cytochrome c protein,downregulated survivin and Bcl-2 protein,and the activation of caspase-3 and ***,Dkk-3 overexpression reduced the accumulation of cytosolic fraction of β-***:Dkk-3 overexpression induced apoptosis in human colon cancer possibly through the mitochondrial ***-3 may be involved in the Wnt/β-catenin signaling pathways in colon cancer.