摘要
目的探讨Wnt信号通路阻滞剂DKK-1对人结肠癌细胞HCT116侵袭能力的影响及其分子机制。方法将HCT116细胞随机分为观察组和对照组,分别给予DKK-1 100 ng/m L及等量细胞培养液继续培养48 h。采用Transwell侵袭实验观测肿瘤细胞侵袭能力的变化,分别采用Western blot法、RT-PCR法检测肿瘤细胞中Wnt信号通路关键基因β-catenin、EMT调控因子Snail及上皮细胞标记物E-cadherin、间质细胞标记物Vimentin的蛋白及mRNA表达,结果观察组穿膜细胞数为(45.29±6.25)个/HP,低于对照组的(76.36±8.32)个/HP,差异有统计学意义(P<0.05)。与对照组比较,观察组HCT116细胞中β-catenin、Snail、Vimentin蛋白及mRNA表达水平均降低,E-cadherin蛋白及mRNA表达水平增高(P均<0.05)。结论 Wnt信号通路阻滞剂DKK-1可能通过抑制肿瘤细胞上皮-间充质转化过程,进而降低人结肠癌细胞HCT116的侵袭能力。
Objective To investigate the effects and molecular mechanism of Writ signal pathway antagonist DKK-1 on invasion ability of colon cancer cell line HCTll6. Methods Conlon cancer HCTll6 cells were divided into the experimental group and control group, which were cultured with exogenous DKK-1 （ 100 ng/mL） and the same amount of cell culture medium for 48 h, respectively. Transwell was used to observe the change of invasion ability. The protein and mRNA expression of β-catenin, Snail, E-cadherin and Vinentin in the HCT116 cells was observed by Western blotting and RT-PCR. Results The number of transmembrane ceils in the experimental group was （45.29 ± 6.25）/HP which was obviously lower than that in control group[ （76.36 ± 8.32）/HP], and the difference was statistically significant （P 〈 0.05 ）. The protein and mRNA expression of β-catenin, Snail and Vinentin was lower and the expression of E-cadherin protein and mRNA was higher in the experimental group than that of the control group, and the differences were statistically significant （ all P 〈 0. 05）. Conclusion Wnt signal pathway antagonist DKK-1 can decrease the invasion ability of conlon cancer cell line HCT116 by inhibiting the process of epithelial-mesenchymal transition in tumor cells.
作者
张延新
张印坡
赵琰
王记红
张艳
崔东涛
ZHANG Yanxin ZHANG Yinpo ZHAO Yan WANG Jihong ZHANG Yan CUI Dongtao(Luohe Medical College, Luohe 462002, China)
出处
《山东医药》
CAS
北大核心
2017年第10期8-10,共3页
Shandong Medical Journal
基金
河南省教育厅青年教师资助项目(2012GGJS-269)
关键词
结肠癌
WNT信号通路
通路阻滞剂
上皮-间充质转化
细胞侵袭
colon carcinoma
Writ signaling pathway
pathway antagonist
epitheIial-mesenchymal transition
cell invasion
