Cancer cell-autonomous TRAIL-R signaling promotes KRAS-driven cancer progression, invasion, and metastasis

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 a...

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Vydané v:Cancer cell Ročník 27; číslo 4; s. 561
Hlavní autori: 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
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 13.04.2015
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ISSN:1878-3686, 1878-3686
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Abstract 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.
AbstractList 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.
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.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.
Author Sansom, Owen J
Nobis, Max
Egberts, Jan-Hendrik
Campbell, Andrew D
Hegedüs, Balazs
Taraborrelli, Lucia
Bergmann, Michael
von Karstedt, Silvia
Kenessey, Istvan
Becker, Thomas
Lemke, Johannes
Montinaro, Antonella
Anderson, Kurt I
Koschny, Ronald
Schweiger, Thomas
Ganten, Tom M
Grosse-Wilde, Anne
Walczak, Henning
El-Bahrawy, Mona A
Kalthoff, Holger
Legler, Karen
Conti, Annalisa
Werner, Jens
Hartwig, Torsten
Coy, Johannes F
Röcken, Christoph
Annewanter, Franka
Bergmann, Frank
Hoetzenecker, Konrad
Trauzold, Anna
Hauser, Charlotte
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  organization: Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6DD, UK; Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy
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  organization: Department of Thoracic Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria; Christian Doppler Laboratory for Cardiac and Thoracic Diagnosis and Regeneration, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria
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  year: 2015
  text: 2015-04-13
  day: 13
PublicationDecade 2010
PublicationPlace United States
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PublicationTitle Cancer cell
PublicationTitleAlternate Cancer Cell
PublicationYear 2015
SSID ssj0016179
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Snippet Many cancers harbor oncogenic mutations of KRAS. Effectors mediating cancer progression, invasion, and metastasis in KRAS-mutated cancers are only incompletely...
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StartPage 561
SubjectTerms Animals
Apoptosis - genetics
Carcinoma, Pancreatic Ductal - genetics
Carcinoma, Pancreatic Ductal - metabolism
Carcinoma, Pancreatic Ductal - pathology
Cell Line, Tumor
Cell Proliferation - genetics
Disease Progression
Female
Humans
Male
Mice
Mice, Inbred C57BL
Mice, SCID
Models, Biological
Neoplasm Invasiveness - genetics
Prognosis
Proto-Oncogene Proteins p21(ras) - genetics
Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism
Receptors, TNF-Related Apoptosis-Inducing Ligand - physiology
Title Cancer cell-autonomous TRAIL-R signaling promotes KRAS-driven cancer progression, invasion, and metastasis
URI https://www.ncbi.nlm.nih.gov/pubmed/25843002
https://www.proquest.com/docview/1673792640
Volume 27
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