目的：探讨miR-26b在乳腺癌细胞中的表达及其对乳腺癌细胞生物学行为的的影响。方法：比较正常乳腺细胞系MCF-10A及乳腺癌细胞系MCF-7中miR-26b的表达差异。以无处理的MCF-7细胞为空白对照，分别检测MCF-7细胞转染miR-26b 模拟物（miR-26b 组）、空质粒（阴性对照组）后的miR-26b表达与增殖、迁移、侵袭能力，以及Foxf2的mRNA与蛋白表达的变化。用双荧光素酶报告系统检测miR-26b对MCF-7细胞中Foxf2转录活性的影响。结果：miR-26b在MCF-7细胞中的表达水平明显低于MCF-10A细胞（P<0.05）。与空白对照组和阴性对照组比较，miR-26b组miR-26b mRNA表达水平明显升高、细胞增殖迁移、侵袭能力明显降低，Foxf2的mRNA和蛋白表达量均明显下调（P<0.05）。转染miR-26b模拟物后，MCF-7细胞中Foxf2-3'UTR的转录活性明显抑制（P<0.05）。结论：miR-26b在乳腺癌细胞中表达降低、增加其表达能抑制乳腺癌细胞的恶性生物学行为，机制可能与其下调Foxf2的表达有关。
Effects of miR-26b expression and its interaction with Foxf2 on the biological behaviors in breast cancer cells
Objective: To investigate the miR-26b expression and its influence on the biological behaviors in breast cancer cells. Methods: The differences of miR-26b expressions in normal breast cell line MCF-10A and breast cancer cell line MCF-7 were compared. Using untreated MCF-7 cells as blank control, the changes in miR-26b expression, abilities of proliferation, migration and invasion, and Foxf2 mRNA and protein expressions in MCF-7 cells after transfection with miR-26b mimics (miR-26b) group or empty plasmid (negative control group) were determined. The influence of miR-26b on transcriptional activity of Foxf2 in MCF-7 cells was determined by dual-luciferase reporter assay system. Results: The miR-26b expression level in MCF-7 cells was significantly lower than that in MCF-10A cells (P<0.05). In miR-26b group compared with the blank control group or negative control group, the miR-26b expression level was significantly increased, the abilities of proliferation, migration and invasion were significantly decreased, and the mRNA and protein expression levels of Foxf2 were significantly down-regulated (all P<0.05). The transcriptional activity of Foxf2-3'UTR was significantly inhibited in MCF-7 cells after miR-26b mimics transfection (P<0.05). Conclusion: MiR-26b expression is decreased in breast cancer cells, increasing its expression can suppress the malignant biological behaviors of breast cancer cells, and the mechanism may be related to its down-regulating Foxf2 expression.