Malignant phenotypes are leading causes of death in patients with breast cancer (BC). Previously, it has been proved that tubulin polymerization promoting protein 3 (TPPP3) participates in cell progressions in several human cancers. Little is known about the functions of TPPP3 in BC. Herein, we detected the expression of TPPP3 in 54 clinical BC tissues and two BC cell lines by immunohistochemistry and Western blot. CCK‐8, wound healing, colony formation and Transwell assays were used to assess cell proliferation, clone formation, invasion and migration of MCF‐7 and T47D cells after transfection with TPPP3 siRNA. Meanwhile, related‐proteins expression was detected using Western blot. TPPP3 was found to be highly expressed in the tissues from the patients with BC. Poor outcomes were associated with the high expression of TPPP3 in all patients with BC. When MCF‐7 and T47D cells receiving TPPP3 siRNA transfection, the capacities of proliferation, clone formation, invasion and migration were suppressed and the expression of MMP‐2/−9 and NF‐κB p65/COX2 was notably reduced. The dual‐luciferase reporter assay indicated that the promoter regions of NF‐κB p65 could combine to TPPP3. Overall, the present study demonstrated that TPPP3 played a significant role in BC, and its inhibition lead to the suppression of NF‐κB/COX‐2 signalling pathway along with the reduction of malignant phenotypes.

中文翻译：

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TPPP3沉默可通过灭活乳腺癌细胞中的NF-κB/ COX2信号通路抑制细胞增殖，侵袭和迁移。

恶性表型是乳腺癌（BC）患者的主要死亡原因。以前，已经证明微管蛋白聚合促进蛋白3（TPPP3）参与了几种人类癌症的细胞进程。关于BC中TPPP3的功能知之甚少。在本文中，我们通过免疫组织化学和Western印迹检测了TPPP3在54个临床BC组织和两个BC细胞系中的表达。用TPPP3 siRNA转染后，使用CCK-8，伤口愈合，集落形成和Transwell分析评估MCF-7和T47D细胞的细胞增殖，克隆形成，侵袭和迁移。同时，使用蛋白质印迹法检测相关蛋白的表达。发现TPPP3在BC患者的组织中高表达。结果差与所有BC患者中TPPP3的高表达有关。当MCF-7和T47D细胞接受TPPP3 siRNA转染时，其增殖，克隆形成，侵袭和迁移的能力受到抑制，MMP-2--9和NF-κBp65 / COX2的表达明显降低。双荧光素酶报告基因检测表明，NF-κBp65的启动子区域可能与TPPP3结合。总体而言，本研究表明，TPPP3在BC中起重要作用，其抑制作用导致NF-κB/ COX-2信号通路的抑制以及恶性表型的减少。双重荧光素酶报告基因测定表明，NF-κBp65的启动子区域可能与TPPP3结合。总体而言，本研究表明，TPPP3在BC中起重要作用，其抑制作用导致NF-κB/ COX-2信号通路的抑制以及恶性表型的减少。双荧光素酶报告基因检测表明，NF-κBp65的启动子区域可能与TPPP3结合。总体而言，本研究表明，TPPP3在BC中起重要作用，其抑制作用导致NF-κB/ COX-2信号通路的抑制以及恶性表型的减少。