摘要
目的探讨趋化因子受体7(CXCR7)在不同分化程度的胃癌细胞系中的表达以及siRNA沉默CXCR7后对胃癌SGC-7901细胞迁移及侵袭能力的影响。方法体外培养5种人胃癌细胞系:未分化腺癌HGC-27、低分化黏液腺癌MGC-803、低分化腺癌BGC-823、中分化腺癌SGC-7901和高分化腺癌MKN-28。采用Western blot及RT-PCR法分别检测CXCR7的蛋白及mRNA表达。应用脂质体转染siRNA的方法沉默SGC-7901细胞CXCR7的表达,并采用其配体基质细胞衍生因子-1(SDF-1)干预,实验分为4组:阴性对照siRNA(NC siRNA组),NC siRNA+SDF-1组,CXCR7siRNA组和CXCR7siRNA+SDF-1组。应用Transwell小室检测细胞迁移及侵袭能力。结果 CXCR7在不同人胃癌细胞系中表达程度不一,其中高分化MKN-28几乎不表达,中分化SGC-7901细胞表达程度最高。与NC siRNA组相比,NC siRNA+SDF-1组的迁移细胞数和侵袭细胞数增加(P<0.05),CXCR7siRNA组的迁移细胞数和侵袭细胞数减少(P<0.05);与NC siRNA+SDF-1组相比,CXCR7siRNA+SDF-1组的迁移细胞数和侵袭细胞数减少(P<0.05)。结论 CXCR7在中分化腺癌细胞系SGC-7901表达程度最高;SGC-7901细胞的迁移和侵袭能力可被SDF-1提升,亦可被CXCR7siRNA抑制。
Objective To determine the expression of chemokine （C-X-C motif） receptor 7 （CXCR7） in five gastric cancer cell lines with various degrees of differentiation, and the effect of silencing CXCR7 on the migration and invasion of SGC-7901 cells. Methods The expression of CXCR7 in gastric cell lines （HGC-27, MGC-803, SGC-7901, BGC-823 and MKN-28） was detected by Western bolt and RT-PCR. The SGC-7901 cells were transfected with liposome of CXCR7 siRNA to silence CXCR7 gene, and then treated with stromal-derived factor-/ （SDF-1） the ligand of CXCR7. Transwell assay was used for determining the migratory and invasive ability of SGC-7901 cells in the four groups： NC siRNA, NC siRNA＋SDF-1, CXCR7 siRNA and CXCR7 siRNA＋SDF-1. Results CXCR7 was expressed in the five gastric cancer cell lines, with the highest intensity in SGC-7901. The migrated and invasive cells increased in the NC siRNA＋ SDF-1 group and reduced in the CXCR7-siRNA group compared with the NC siRNA group （PM0.05）. The CXCR7-siRNA＋SDF-1 group had less migrated and invasive cells than the NC siRNA-I-SDF-1 group （P〈0.05）. Conclusion CXCR7 is highly expressed in SGC-7901. SDF-1 promotes the migratory and invasive capability of SGC-7901 cells, but such an effect can be inhibited by silencing it with CXCR7 siRNA .
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2016年第5期685-690,共6页
Journal of Sichuan University(Medical Sciences)
基金
国家星火计划(No.2011GAB50001)资助
