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题目:: Cancer cell-autonomous TRAIL-R signaling promotes KRAS-driven cancer progression, invasion, and metastasis.
作者:: von Karstedt(Silvia),Conti(Annalisa),Nobis(Max),Montinaro(Antonella),Hartwig(Torsten),Lemke(Johannes),Legler(Karen),Annewanter(Franka),Campbell(Andrew D),Taraborrelli(Lucia),Grosse-Wilde(Anne),Coy(Johannes F),El-Bahrawy(Mona A),Bergmann(Frank),Koschny(Ronald),Werner(Jens),Ganten(Tom M),Schweiger(Thomas),Hoetzenecker(Konrad),Kenessey(Istvan),Hegedüs(Balazs),Bergmann(Michael),Hauser(Charlotte),Egberts(Jan-Hendrik),Becker(Thomas),Röcken(Christoph),Kalthoff(Holger),Trauzold(Anna),Anderson(Kurt I),Sansom(Owen J),Walczak(Henning)
状态:: 发布时间2015-04-15 , 更新时间 2016-11-22
期刊:: Cancer Cell
摘要:: Many cancers harbor oncogenic mutations of KRAS. Effectors mediating cancer progression, invasion, and metastasis in KRAS-mutated cancers are only incompletely understood. Here we identify cancer cell-expressed murine TRAIL-R, whose main function ascribed so far has been the induction of apoptosis as a crucial mediator of KRAS-driven cancer progression, invasion, and metastasis and in vivo Rac-1 activation. Cancer cell-restricted genetic ablation of murine TRAIL-R in autochthonous KRAS-driven models of non-small-cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) reduces tumor growth, blunts metastasis, and prolongs survival by inhibiting cancer cell-autonomous migration, proliferation, and invasion. Consistent with this, high TRAIL-R2 expression correlates with invasion of human PDAC into lymph vessels and with shortened metastasis-free survival of KRAS-mutated colorectal cancer patients.
语言:: eng
DOI:: 10.1016/j.ccell.2015.02.014

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