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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2017,12,26]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>Current cancer therapies fail to repress tumor recurrence and metastasis in triple-negative breast cancer (TNBC) because they fail to target cells that possess epithelial\u2013mesenchymal (E-M) plasticity and acquire cancer stem cell (CSC) properties. Identifying and engaging signaling pathways that regulate E-M\/CSC plasticity within TNBC therefore remains an unmet critical clinical need. Recent evidence demonstrates that presence of E-M\/CSC plasticity in TNBC correlates with a repressed interferon\/STAT gene signature. Our data demonstrate that exogenous IFN-\u03b2 targets and represses E-M\/CSC plasticity by reengaging type I IFN signaling in CSC. Our findings have clinical relevance, as IFN-\u03b2 signaling correlates with improved patient survival and repressed CSC in TNBC. 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