TNF-α increases breast cancer stem-like cells through up-regulating TAZ expression via the non-canonical NF-κB pathway
TNF-α increases breast cancer stem-like cells through up-regulating TAZ expression via the non-canonical NF-κB pathway
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TNF-α 通过非经典 NF-kappa B 途径上调 TAZ 表达来增加乳腺癌干样细胞
DOI：
10.1038/s41598-020-58642-y
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发表时间：
2020-02-04
影响因子：
4.6
通讯作者：
Chen, Ceshi
中科院分区：
文献类型：
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作者：
Liu, Wenjing;Lu, Xiaoqing;Chen, Ceshi
乳腺癌患者经常由于乳腺癌干细胞样细胞（BCSC）的存在而遭受疾病复发和转移。许多研究已经报道了高水平的炎症因子，包括肿瘤坏死因子α（TNF-α），促进BCSC。然而，TNF-α促进BCSC的机制尚不清楚。在这项研究中，我们证明了TNF-α上调TAZ，一种促进人类乳腺癌细胞系BCSC自我更新能力的转录辅激活因子。TAZ的消耗消除了由TNF-α介导的BCSC的增加。TAZ是由TNF-α通过非经典的NF-κ B通路诱导的，我们的研究结果表明，TAZ在炎症因子促进的乳腺癌干细胞中起着至关重要的作用，并可能作为一个有前途的治疗靶点。
Breast cancer patients often suffer from disease relapse and metastasis due to the presence of breast cancer stem-like cells (BCSCs). Numerous studies have reported that high levels of inflammatory factors, including tumor necrosis factor alpha (TNF-alpha), promote BCSCs. However, the mechanism by which TNF-alpha promotes BCSCs is unclear. In this study, we demonstrate that TNF-alpha up-regulates TAZ, a transcriptional co-activator promoting BCSC self-renewal capacity in human breast cancer cell lines. Depletion of TAZ abrogated the increase in BCSCs mediated by TNF-alpha. TAZ is induced by TNF-alpha through the non-canonical NF-kappa B pathway, and our findings suggest that TAZ plays a crucial role in inflammatory factor-promoted breast cancer stemness and could serve as a promising therapeutic target.