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目的:探讨不同乳腺癌细胞株Stat6活化分型的可行性及IL-4的作用机制。方法:流式细胞仪测定不同Stat6表型细胞株ZR-75-1和BT-20的早期凋亡率;应用Affymetrix基因芯片测定IL-4刺激前后的基因表达谱变化。结果:Stat6null表型细胞与Stat6high相比早期凋亡增加(40%vs12%);在Stat6null细胞株有2193个基因/转录产物表达升高,而Stat6high细胞株中2600个基因/转录产物表达升高,且Stat6high细胞和Stat6null细胞中与凋亡和转移相关的基因表达谱明显不同;但不论在Stat6high还是Stat6null细胞株,IL-4均上调CCL26、SOCS1、CISH、EGLN3和SIDT1基因,而下调DUSP1、FOS和FOSB基因。结论:在乳腺癌细胞中,IL-4可能像在免疫细胞中一样,通过Stat6或非Stat6途径而发挥功能。
Objective: To investigate the feasibility of Stat6 activation typing in different breast cancer cell lines and the mechanism of action of IL-4. METHODS: Flow cytometry was used to determine the early apoptotic rate of different Stat6 phenotype cell lines ZR-75-1 and BT-20. The gene expression profile before and after IL-4 stimulation was measured by Affymetrix gene chip. Results: Stat6null phenotypic cells showed an increase in early apoptosis compared with Stat6high (40% vs 12%); 2193 genes/transcripts were up-regulated in Stat6null cell lines, and 2600 genes/transcripts were upregulated in Stat6high cell lines. The expression patterns of genes related to apoptosis and metastasis in Stat6high cells and Stat6null cells are significantly different. However, in Stat6high or Stat6null cell lines, IL-4 upregulates CCL26, SOCS1, CISH, EGLN3, and SIDT1 genes and DUSP1 is down-regulated. FOS and FOSB genes. CONCLUSIONS: In breast cancer cells, IL-4 may function through the Stat6 or non-Stat6 pathway as it does in immune cells.