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

被引:97
作者
Liu, Wenjing [1 ,2 ,3 ]
Lu, Xiaoqing [4 ]
Shi, Peiguo [1 ]
Yang, Guangxi [1 ]
Zhou, Zhongmei [1 ]
Li, Wei [3 ,5 ]
Mao, Xiaoyun [6 ]
Jiang, Dewei [1 ]
Chen, Ceshi [1 ,7 ]
机构
[1] Chinese Acad Sci, Key Lab Anim Models & Human Dis Mech, Chinese Acad Sci & Yunnan Prov, Kunming Inst Zool, Kunming 650223, Yunnan, Peoples R China
[2] Univ Chinese Acad Sci, Beijing 101407, Peoples R China
[3] Kunming Univ Sci & Technol, Med Fac, Kunming 650500, Yunnan, Peoples R China
[4] Shanxi Med Univ, Dept Breast Surg, Hosp 2, Taiyuan 030071, Peoples R China
[5] First Peoples Hosp Yunnan Prov, Dept Urol, Kunming 650032, Yunnan, Peoples R China
[6] China Med Univ, Affiliated Hosp 1, Breast Surg, Shenyang 110001, Peoples R China
[7] Chinese Acad Sci, Kunming Inst Zool, KIZ CUHK Joint Lab Bioresources & Mol Res Common, Kunming, Yunnan, Peoples R China
关键词
TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR; TRANSCRIPTION; INFLAMMATION; PROLIFERATION; CONFERS; MEDIATE; CD44; CD24; GENE;
D O I
10.1038/s41598-020-58642-y
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页数:11
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