核心蛋白聚糖抑制结直肠腺癌细胞系HCT116的体外侵袭

目的探讨常氧和低氧条件下核心蛋白聚糖(DCN)对结直肠腺癌细胞系HCT116体外侵袭的作用及机制。方法 Transwell法检测HCT116细胞体外侵袭能力;Real-time PCR法检测细胞CD133和TIMP-2 mRNA的表达;Western blot检测细胞HIF-1α、CD133和TIMP-2蛋白的表达。结果 1)常氧和低氧环境下,DCN浓度为0、1和3mg/L时HCT116细胞的侵袭数量分别为(241±46)、(168±46)和(51±17)个/视野(P0.01)及(207±61)、(213±64)、(156±54)和(44±17)个/视野(P0.01)。2)在常氧条件下,DCN(3 mg/L)显著上调HCT116细胞TIMP-2mRNA和蛋白的表达(P0.01),而对CD133 mRNA和蛋白的表达无明显作用。3)低氧条件下DCN(3 mg/L)显著下调HCT116细胞HIF-1α/CD133/TIMP-2蛋白的表达(P0.01),而对CD133 mRNA的表达无明显影响。结论DCN抑制结直肠腺癌细胞HCT116体外侵袭能力,在常氧和低氧条件下可能通过不同机制发挥作用。

Inhibitory effect of decorinon invasion of colorectal adenocarcinoma cell line HCT116 in vitro

Objective To investigate the effect and mechanism of decorin (DCN) on invasion of colorectal cancer cell line HCT116 in vitro.Methods Transwell assay was employed to detect the invasion of HCT116 cells;Real-time PCR was used to detect the expression of CD133 and TIMP-2 mRNA of HCT116 cells;Western blot method was used to detect the expression of HIF-1α, CD133 and TIMP-2 protein of HCT116 cells.Results 1) When the concentrations of DCN was 0, 1 and 3 mg/L, under the conditions of normal oxygen and hypoxia, the numbers of invasive cells were (241±46), (168±46), (51±17) fields in each well (P<0.01) and (207±61), (213±64), (156±54), (44±17) fields in each well (P<0.01).2) Under the normoxic conditions, the TIMP-2 mRNA and protein in HCT116 cells were increased by DCN (3 mg/L) (P<0.01), but that of CD133 were not affected.3) DCN (3 mg/L) significantly decreased the expression of HIF-1α/CD133/TIMP-2 protein in HCT116 cells under hypoxia (P<0.01), but had no significant effect on the expression of CD133 mRNA.ConclusionsUnder the conditions of hypoxia and normal oxygen, DCN may function through different mechanisms to inhibit the invasion of colorectal adenocarcinoma cell line HCT116 in vitro.