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目的:观察长链非编码RNA(lncRNA)叉头框蛋白C1(FOXC1)基因启动子上游转录体(FOXCUT)调控JAK信号在乳腺癌细胞增殖、迁移和侵袭中的作用。方法:采用实时定量反转录聚合酶链反应(qRT-PCR)检测lncRNA FOXCUT在乳腺癌细胞株(MCF-7和MDA-MB-231)和人正常乳腺上皮细胞(MCF-10A)中的表达。体外干扰lncRNA-FOXCUT在乳腺癌细胞MCF-7中表达，利用细胞计数试剂盒(CCK-8)法、伤口愈合法和细胞侵袭实验检测lncRNA FOXCUT对乳腺癌细胞增殖、迁移和侵袭的影响。同时，用qRT-PCR和蛋白质印迹法(Western blot)检测B细胞淋巴瘤2(bcl-2)、基质金属蛋白酶-9(MMP-9)和Janus激酶1(JAK1)、信号转导和转录激活因子3(STAT3)的表达。多组间比较采用单因素方差分析，两两比较采用SNK-n q检验。n 结果:lncRNA FOXCUT在乳腺癌细胞MCF-7(1.567±0.270，n t＝5.086，n P<0.01)和MDA-MB-231(1.513±0.387，n t＝3.533，n P<0.01)中表达明显高于MCF-10A细胞(1.004±0.193)，差异有统计学意义。siRNA-FOXCUT组细胞增殖活力明显低于NC组(48 h时0.790±0.068比0.991±0.165，n t＝2.516，n P<0.05；72 h时0.928±0.135比1.500±0.311，n t＝3.775，n P<0.01)，差异有统计学意义。同时，siRNA-FOXCUT组MCF-7细胞的迁移率[(30.163±4.133)%比(79.330±4.952)%，n t＝13.200，n P<0.01]和侵袭[(101.000±13.115)个比(244.667±18.771)个，n t＝10.870，n P<0.01]能力均低于NC组，差异有统计学意义。siRNA-FOXCUT组细胞中bcl-2(0.565±0.058比1.075±0.242，n t＝3.555，n P<0.01)和MMP-9(0.527±0.138比0.982±0.172，n t＝3.574，n P<0.01)在mRNA和蛋白水平均低于NC组，同时p-JAK1(0.185±0.031比1.095±0.134，n t＝11.460，n P<0.01)和p-STAT3(0.298±0.029比0.948±0.235，n t＝4.755，n P<0.01)蛋白表达低于NC组，差异有统计学意义。n 结论:lncRNA FOXCUT可能通过JAK1/STAT3途径参与调控乳腺癌的增殖、迁移和侵袭。“,”Objective:To investigate the role of long non-coding RNA (lncRNA) forkhead box c1 promoter upstream transcript (FOXCUT) in proliferation, migration and invasion of breast cancer cells.Methods:The expression of lncRNA FOXCUT in breast cancer cell lines [michigan cancer foundation 7(MCF-7) and : MD anderson metastatic breast cancer 231(MDA-MB-231)] and human normal michigan cancer foundation 10A (MCF-10A) was detected by real-time quantitative reverse transcription-polymerase chain reactions (qRT-PCR). The expression of lncRNA FOXCUT was silenced in MCF-7 cells, and proliferation, migration and invasion abilities were measured using cell counting kit-8 (CCK-8), Wound-healing and transwell assays. The expression of B-cell lymphoma-2 (bcl-2), matrix metallopeptidase-9 (MMP-9) and janus kinase-1 (JAK1), signal transducer and activator of transcription-3 (STAT3) was detected by qRT-PCR and Western blotting. One-way ANOVA was used for multiple comparisons, and student-Newman-Keuls (SNK)-q test was used for comparison of selected two groups.Results:LncRNA FOXCUT was significantly upregulated in breast cancer cells MCF-7 (1.567±0.270, n t=5.086, n P<0.01) and MDA-MB-231 (1.513±0.387,n t=3.533, n P<0.01) as compared with MCF-10A cells (1.004±0.193). The cell proliferation ability was decreased in siRNA-FOXCUT group as compared with normal control(NC) group (0.790±0.068 vs. 0.991±0.165,n t=2.516, n P<0.05 at 48 h; 0.928±0.135 vs. 1.500±0.311,n t=3.775, n P<0.01 at 72 h). The down-expression of lncRNA FOXCUT had lower migration [(30.163±4.133)% vs. (79.330±4.952)%,n t=13.200, n P<0.01] and invasion [(101.000±13.115) cells vs. (244.667±18.771) cells,n t=10.870, n P<0.01]) abilities than NC group. SiRNA-FOXCUT significantly inhibited the bcl-2 (0.565±0.058 vs. 1.075±0.242,n t=3.555, n P<0.01) and MMP-9 (0.527±0.138 vs. 0.982±0.172,n t=3.574, n P<0.01) on both mRNA and protein levels. Down-expression of lncRNA FOXCUT significantly inhibited the protein level of p-JAK1 (0.185±0.031 vs. 1.095±0.134,n t=11.460, n P<0.01) and p-STAT3 (0.298±0.029 vs. 0.948±0.235,n t=4.755, n P<0.01).n Conclusion:LncRNA FOXCUT may be functionally involved in the proliferation, migration and invasion of breast cancer cells through the regulation of JAK1/STAT3 pathway, demonstrating that lncRNA FOXCUT may serve as a novel biomarker and therapeutic target in breast cancer.