BACKGROUND Breast cancer is the second common malignant cancer among females worldwide. Accumulating studies have indicated that deregulation of miRNA expression in breast cancer will contribute to tumorigenesis and form different cancer subtypes. However, the reported studies on miR-29b-3p-regulated breast cancer are limited so far. Herein, we investigated the role and mechanism of miR-29b-3p in the triple negative breast cancer cell line MDA-MB-231. METHODS The relative miR-29b-3p expression in different breast cancer cell lines were determined by qRT-PCR. CCK8 and colony formation assay were used to determine the influence of miR-29b-3p on cell proliferation. Migration assay and invasion assay were performed for cell migration and invasion respectively. To study the cell integrity immunofluorescence was performed. TUNEL assay, flow cytometry assay, hoechst staining and western blot were conducted to determine the influence of miR-29b-3p inhibitor on cell apoptosis. TRAF3 was found to be the target gene of miR-29b-3p using bioinformatics predictions. Dual-luciferase assay was performed to determine the relative luciferase activity in NC, miR-29b-3p mimic, miR-29b-3p inhibitor with TRAF3 3'-UTR wt or TRAF3 3'-UTR mt reporter plasmids. The proteins expression of NF-κB signaling pathway in MDA-MB-231 after transfection with NC, miR-29b-3p mimic, miR-29b-3p inhibitor were determined by western blot. RESULTS The miR-29b-3p expression was significantly increased in MDA-MB-231 compare with MCF-10A. miR-29b-3p inhibitor reduced the cell viability of MDA-MB-231 and inhibited cell migration and invasion. Cell cytoskeleton integrity destroyed after miR-29b-3p inhibitor treatment. Furthermore, we identified the mechanism and found miR-29b-3p targets the TRAF3 and activates NF-κB signaling pathway. CONCLUSIONS From the above studies, our results indicated that miR-29b-3p acts as a promoter for the development of MDA-MB-231.

中文翻译：

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miR-29b-3p 通过下调 TRAF3 促进 MDA-MB-231 三阴性乳腺癌细胞的进展。

背景技术乳腺癌是全世界女性第二常见的恶性肿瘤。越来越多的研究表明，乳腺癌中miRNA表达的失调将有助于肿瘤发生并形成不同的癌症亚型。然而，迄今为止关于miR-29b-3p调节的乳腺癌的研究报道有限。在此，我们研究了 miR-29b-3p 在三阴性乳腺癌细胞系 MDA-MB-231 中的作用和机制。方法通过qRT-PCR测定不同乳腺癌细胞系中miR-29b-3p的相对表达量。CCK8和集落形成实验用于确定miR-29b-3p对细胞增殖的影响。分别对细胞迁移和侵袭进行迁移实验和侵袭实验。为了研究细胞完整性，进行了免疫荧光。采用TUNEL实验、流式细胞仪实验、Hoechst染色和Western blot检测miR-29b-3p抑制剂对细胞凋亡的影响。通过生物信息学预测发现TRAF3是miR-29b-3p的靶基因。进行双荧光素酶测定以确定 NC、miR-29b-3p 模拟物、miR-29b-3p 抑制剂与 TRAF3 3'-UTR wt 或 TRAF3 3'-UTR mt 报告质粒的相对荧光素酶活性。Western blot检测转染NC、miR-29b-3p模拟物、miR-29b-3p抑制剂后MDA-MB-231中NF-κB信号通路蛋白的表达。结果与MCF-10A相比，MDA-MB-231中miR-29b-3p的表达显着增加。miR-29b-3p抑制剂降低MDA-MB-231的细胞活力并抑制细胞迁移和侵袭。miR-29b-3p 抑制剂处理后细胞骨架完整性被破坏。此外，我们确定了其机制并发现 miR-29b-3p 靶向 TRAF3 并激活 NF-κB 信号通路。结论 从上述研究中，我们的结果表明 miR-29b-3p 充当 MDA-MB-231 发育的启动子。