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

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.