TNF-α 通过非经典 NF-κB 通路上调 TAZ 表达增加乳腺癌干细胞样细胞。
TNF-α increases breast cancer stem-like cells through up-regulating TAZ expression via the non-canonical NF-κB pathway.
机构信息
Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China.
University of the Chinese Academy of Sciences, Beijing, 101407, China.
出版信息
Sci Rep. 2020 Feb 4;10(1):1804. doi: 10.1038/s41598-020-58642-y.
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-α), promote BCSCs. However, the mechanism by which TNF-α promotes BCSCs is unclear. In this study, we demonstrate that TNF-α 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-α. TAZ is induced by TNF-α through the non-canonical NF-κB 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.
乳腺癌患者常因存在乳腺癌干细胞样细胞（BCSCs）而遭受疾病复发和转移。大量研究报道，高水平的炎症因子，包括肿瘤坏死因子α（TNF-α），促进了 BCSCs。然而，TNF-α 促进 BCSCs 的机制尚不清楚。在这项研究中，我们证明 TNF-α 上调了 TAZ，一种转录共激活因子，促进了人乳腺癌细胞系中 BCSC 的自我更新能力。TAZ 的耗竭消除了 TNF-α介导的 BCSC 增加。TAZ 是由 TNF-α 通过非经典 NF-κB 途径诱导的，我们的研究结果表明 TAZ 在炎症因子促进的乳腺癌干细胞特性中起关键作用，并且可能成为有前途的治疗靶标。
Zotero 插件