Triple-negative breast cancer (TNBC) has special characteristics of significant aggressiveness, and strong potential for metastasis and recurrence; currently there are no targeted drugs for TNBC. Abnormal activation of epithelial-mesenchymal transition (EMT) plays an important role in these malignant behaviors of TNBC. In the crosstalk among the multiple EMT-associated signaling pathways, many miRNAs participate in regulating pathway activity, where they act as "traffic lights" at the intersection of these pathways. In this study, we used miRNA microarray technology to detect differentially expressed miRNAs related to EMT in TNBC, and we identified and verified 9 highly expressed oncogenic miRNAs (OncomiRs). High expression of these OncomiRs in clinical breast cancer tissues affected the prognosis of patients, and inhibition of their expression blocked EMT in TNBC cell lines and suppressed cancer cell proliferation and migration. We constructed an oncolytic adenovirus (AdSVP-lncRNAi9) armed with an artificially-designed interfering lncRNA (lncRNAi9), which exhibited an activity to block EMT in TNBC cells by disrupting the functions of multiple OncomiRs; the efficacy of such a treatment for TNBC was demonstrated in cytology and animal experiments. This research provides a new candidate oncolytic virotherapy for treating highly malignant refractory TNBC.

三阴性乳腺癌（TNBC）具有侵袭性强，转移和复发潜力大的特点。目前尚无针对TNBC的靶向药物。上皮-间质转化（EMT）的异常激活在TNBC的这些恶性行为中起重要作用。在多个与EMT相关的信号通路之间的串扰中，许多miRNA参与调节通路的活性，在这些通路的交汇处，它们充当“交通灯”。在这项研究中，我们使用miRNA芯片技术检测TNBC中与EMT相关的差异表达的miRNA，并鉴定并验证了9种高表达的致癌性miRNA（OncomiRs）。这些OncomiR在临床乳腺癌组织中的高表达影响了患者的预后，抑制它们的表达可阻断TNBC细胞系中的EMT，并抑制癌细胞的增殖和迁移。我们构建了带有人为设计的干扰lncRNA（lncRNAi9）的溶瘤腺病毒（AdSVP-lncRNAi9），其通过破坏多个OncomiRs的功能表现出阻断TNBC细胞EMT的活性。细胞学和动物实验证明了这种治疗TNBC的功效。这项研究提供了一种新的候选溶瘤病毒疗法来治疗高度恶性的难治性TNBC。通过破坏多个OncomiRs的功能表现出阻断TNBC细胞EMT的活性；细胞学和动物实验证明了这种治疗TNBC的功效。这项研究提供了一种新的候选溶瘤病毒疗法来治疗高度恶性的难治性TNBC。通过破坏多个OncomiRs的功能表现出阻断TNBC细胞EMT的活性；细胞学和动物实验证明了这种治疗TNBC的功效。这项研究提供了一种新的候选溶瘤病毒疗法来治疗高度恶性的难治性TNBC。