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目的探讨趋化因子受体CXCR4异质性在人肺癌(Human Lung Cancer,简称HLC)转移机制中的作用。方法以免疫组织化学方法检测HLC组织中CXCR4蛋白表达水的表达;通过原代培养HLC细胞,进行流式细胞仪分选出CXCR4+HLC细胞和CXCR4-HLC细胞两个亚群。利用Transwell小室法,检测两个亚群细胞的体外侵袭力;检侧CX-CL12和CXCR4的拮抗剂AMD 3100对CXCR4+HLC细胞和CXCR4-HLC细胞体外侵袭能力的影响。结果免疫组化检查提示肺癌组织中CXCR4阳性表达51例,阳性表达率为60.7%;经流式细胞仪检查CXCR4阳性表达率为89.4%;Transwell侵袭实验结果显示,CXCR4+HLC细胞穿过基底膜的细胞数为(34.07±7.05)个,CXCR4-HLC细胞仅为(17.60±4.01)个。CXCR4+HLC细胞体外侵袭能力明显强于CXCR4-HLC细胞(P<0.05,差异有统计学意义);CX-CR4+HLC细胞株+CXCL12(30 ng/ml)穿过基底膜的细胞数为(67.60±3.87)个,显著低于CXCR4+HLC细胞株+CX-CL12 100 ng/ml组,其穿膜细胞数为(106.1±24.2)个(P<0.05,差异有统计学意义);CXCL12(100 ng/ml)+AMD3100组仅为(24.53±5.50)。AMD3100组与另两组比较有统计学意义(P<0.05)。结论人肺癌组织中CXCR4表达存在异质性;趋化因子CXCL12可促进CXCR4表达阳性的肺癌细胞侵袭活性,而CXCR4的抑制剂AMD3100能抑制这种侵袭活性。
Objective To investigate the role of chemokine receptor CXCR4 heterogeneity in metastasis of human lung cancer (HLC). Methods The expression of CXCR4 protein in HLC tissues was detected by immunohistochemical method. Two subpopulations of CXCR4 + HLC cells and CXCR4-HLC cells were sorted by primary culture of HLC cells by flow cytometry. Transwell chamber assay was used to detect the in vitro invasiveness of two subpopulations. The effects of CX31CL and CXCR4 antagonist AMD 3100 on the invasiveness of CXCR4 + HLC cells and CXCR4-HLC cells in vitro were detected. Results The expression of CXCR4 in lung cancer tissues was detected by immunohistochemistry in 51 cases, the positive rate was 60.7%. The positive rate of CXCR4 was 89.4% by flow cytometry. Transwell invasion assay showed that CXCR4 + HLC cells penetrated the basement membrane (34.07 ± 7.05) cells and only CXCR4-HLC cells (17.60 ± 4.01). CXCR4 + HLC cells in vitro invasion was significantly stronger than CXCR4-HLC cells (P <0.05, the difference was statistically significant); CX-CR4 + HLC cell line + CXCL12 (30 ng / ml) through the basement membrane cell number 67.60 ± 3.87), which was significantly lower than CXCL4 + HLC cell line + CX-CL12 100 ng / ml group (106.1 ± 24.2) (P <0.05, the difference was statistically significant); CXCL12 100 ng / ml) + AMD3100 group was only (24.53 ± 5.50). AMD3100 group and the other two groups were statistically significant (P <0.05). Conclusions The expression of CXCR4 in human lung cancer is heterogeneous. Chemokine CXCL12 can promote the invasiveness of CXCR4-positive lung cancer cells, while CXCR4 inhibitor AMD3100 can inhibit this invasiveness.