CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response
Abdul S. Qadir(Northwestern University), Paolo Ceppi(Northwestern University), Sonia Brockway(Northwestern University), Calvin Law(Northwestern University), Liang Mu(Northwestern University), Nikolai N. Khodarev(University of Chicago), Jung Kim(Northwestern University), Jonathan C. Zhao(Northwestern University), William Putzbach(Northwestern University), Andrea E. Murmann(Northwestern University), Zhuo Chen(Center for Cancer Research), Wenjing Chen(Case Western Reserve University), Xia Liu(Northwestern University), Arthur R. Salomon(Center for Cancer Research), Huiping Liu(Case Western Reserve University), Ralph R. Weichselbaum(University of Chicago), Jindan Yu(Northwestern University), Marcus E. Peter(Northwestern University)
Cited by 111Open Access
Abstract
-expressing glioblastoma neurospheres. CD95 stimulation of cancer cells induced secretion of type I interferons (IFNs) that bind to type I IFN receptors, resulting in activation of Janus-activated kinases, activation of STAT1, and induction of a number of STAT1-regulated genes that are part of a gene signature recently linked to therapy resistance in five primary human cancers. Consequently, we identified type I IFNs as drivers of cancer stemness. Knockdown or knockout of STAT1 resulted in a strongly reduced ability of CD95L or type I IFN to increase cancer stemness. This identifies STAT1 as a key regulator of the CSC-inducing activity of CD95.
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