目的·探究三氯生（triclosan，TCS）暴露对三阴性乳腺癌（triple-negative breast cancer，TNBC）进展的影响及其可能的作用机制。方法·采用细胞计数试剂盒8（cell counting kit-8，CCK-8）检测TCS对TNBC细胞MDA-MB-231的半数抑制浓度，以筛选TCS的暴露浓度。分别采用划痕实验、Transwell细胞侵袭实验检测TCS对MDA-MB-231细胞的迁移与侵袭能力的影响。采用实时荧光定量PCR（quantitative real-time PCR，qPCR）检测TCS对MDA-MB-231细胞中miR-21表达的影响，蛋白质印迹法（Western blotting）检测TCS对MDA-MB-231细胞上皮-间质转化（epithelial-mesenchymal transition，EMT）相关蛋白［E-钙黏蛋白（E-cadherin，E-cad）、波形蛋白（vimentin）］的影响。利用免疫组织化学技术与蛋白质印迹法检测TCS暴露对miR-21/STAT3（信号转导和转录活化因子3，signal transducer and activator of transcription 3）信号通路的影响；同时，对MDA-MB-231细胞转染miR-21 mimics，检测TCS暴露对该细胞的迁移与侵袭能力的影响。结果·根据CCK-8实验结果，筛选出TCS的暴露浓度为0.001、0.01、0.1和1 μmol/L。划痕实验与Transwell细胞侵袭实验的结果均显示，0.01、0.1、1 μmol/L TCS暴露均可增强MDA-MB-231细胞的迁移、侵袭能力（均P<0.05）。qPCR的结果表明，0.01、0.1、1 μmol/L TCS暴露后miR-21在TNBC细胞的表达水平均有所下降（均P<0.05）。蛋白质印迹法的结果显示，0.1、1 μmol/L TCS均可下调上皮细胞标志物E-cad的表达，0.01、0.1、1 μmol/L TCS均可上调间叶细胞标志物vimentin的表达（均P<0.05）。免疫组织化学与蛋白质印迹法的结果显示，0.01、0.1、1 μmol/L TCS暴露均可增加STAT3的磷酸化，且呈现剂量依赖效应（均P<0.05）。转染miR-21 mimics上调miR-21的表达后，TCS促进TNBC细胞迁移与侵袭的能力均受到了抑制（均P<0.05）。结论·TCS暴露可通过miR-21/STAT3 信号轴增强TNBC细胞的迁移与侵袭，提示TCS暴露可能对TNBC的进展产生促进效应。

Objective ·To investigate the effect of triclosan (TCS) exposure on the progression of triple-negative breast cancer (TNBC) and to explore the underlying mechanism. Methods ·Cell counting kit-8 (CCK-8) assay was used to detect the half-maximal inhibitory concentration of TCS in the TNBC cell line MDA-MB-231 to screen the exposure concentrations of TCS. The effects of TCS on the migration and invasion abilities of MDA-MB-231 cells were detected by wound-healing assay and Transwell invasion assays, respectively. The effect of TCS on miR-21 expression in MDA-MB-231 cells was detected by quantitative real-time PCR (qPCR). The effects of TCS on the expression of epithelial-mesenchymal transition (EMT)-related proteins, including E-cadherin (E-cad) and vimentin in MDA-MB-231 cells, were detected by Western blotting. The effect of TCS exposure on the miR-21/signal transducer and activator of transcription 3 (STAT3) signaling pathway were detected by immunohistochemistry and Western blotting. Meanwhile, miR-21 mimics were transfected into MDA-MB-231 cells to examine the effects of TCS exposure on the migration and invasion of the cells. Results ·According to the CCK-8 assay, the exposure concentrations of TCS were screened to be 0.001, 0.01, 0.1, and 1 μmol/L. Wound-healing assay and Transwell invasion assay both showed that exposure to 0.01, 0.1, and 1 μmol/L TCS enhanced the migration and invasion abilities of MDA-MB-231 cells (all P<0.05). qPCR results indicated that the expression level of miR-21 in TNBC cells was decreased after exposure to 0.01, 0.1, and 1 μmol/L TCS (all P<0.05). Western blotting results revealed that 0.1 and 1 μmol/L TCS downregulated the expression of the epithelial marker E-cad, and 0.01, 0.1, and 1 μmol/L TCS upregulated the expression of the mesenchymal marker vimentin (all P<0.05). Immunohistochemistry and Western blotting results demonstrated that exposure to 0.01, 0.1, and 1 μmol/L TCS increased the phosphorylation of STAT3 in a dose-dependent manner (all P<0.05). Upregulation of miR-21 by transfection with miR-21 mimics attenuated the promoting effect of TCS on the migration and invasion of TNBC cells (both P<0.05). Conclusion ·TCS exposure enhances the migration and invasion of TNBC cells via the miR-21/STAT3 signaling axis, suggesting that TCS exposure may exert a promoting effect on the progression of TNBC.