TNF-α increases breast cancer stem-like cells through up-regulating TAZ expression via the non-canonical NF-κB pathway.

Wenjing Liu, Xiaoqing Lu, Peiguo Shi, Guangxi Yang, Zhongmei Zhou, Wei Li, Xiaoyun Mao, Dewei Jiang, Ceshi Chen

Scientific reports 2020 Feb 04

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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.

Citation

Wenjing Liu, Xiaoqing Lu, Peiguo Shi, Guangxi Yang, Zhongmei Zhou, Wei Li, Xiaoyun Mao, Dewei Jiang, Ceshi Chen. TNF-α increases breast cancer stem-like cells through up-regulating TAZ expression via the non-canonical NF-κB pathway. Scientific reports. 2020 Feb 04;10(1):1804