Research ExplorerPublicationsEndothelial Notch1 Activity Facilitates Metastasis

Endothelial Notch1 Activity Facilitates Metastasis

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Endothelial Notch1 Activity Facilitates Metastasis. / Wieland, Elfriede; Rodriguez-Vita, Juan; Liebler, Sven S; Mogler, Carolin; Moll, Iris; Herberich, Stefanie E; Espinet, Elisa; Herpel, Esther; Menuchin, Amitai; Chang-Claude, Jenny; Hoffmeister, Michael; Gebhardt, Christoffer; Brenner, Hermann; Trumpp, Andreas; Siebel, Christian W; Hecker, Markus; Utikal, Jochen; Sprinzak, David; Fischer, Andreas.

In: CANCER CELL, Vol. 31, No. 3, 13.03.2017, p. 355-367.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wieland, E, Rodriguez-Vita, J, Liebler, SS, Mogler, C, Moll, I, Herberich, SE, Espinet, E, Herpel, E, Menuchin, A, Chang-Claude, J, Hoffmeister, M, Gebhardt, C, Brenner, H, Trumpp, A, Siebel, CW, Hecker, M, Utikal, J, Sprinzak, D & Fischer, A 2017, 'Endothelial Notch1 Activity Facilitates Metastasis', CANCER CELL, vol. 31, no. 3, pp. 355-367. https://doi.org/10.1016/j.ccell.2017.01.007

APA

Wieland, E., Rodriguez-Vita, J., Liebler, S. S., Mogler, C., Moll, I., Herberich, S. E., Espinet, E., Herpel, E., Menuchin, A., Chang-Claude, J., Hoffmeister, M., Gebhardt, C., Brenner, H., Trumpp, A., Siebel, C. W., Hecker, M., Utikal, J., Sprinzak, D., & Fischer, A. (2017). Endothelial Notch1 Activity Facilitates Metastasis. CANCER CELL, 31(3), 355-367. https://doi.org/10.1016/j.ccell.2017.01.007

Vancouver

Wieland E, Rodriguez-Vita J, Liebler SS, Mogler C, Moll I, Herberich SE et al. Endothelial Notch1 Activity Facilitates Metastasis. CANCER CELL. 2017 Mar 13;31(3):355-367. https://doi.org/10.1016/j.ccell.2017.01.007

Bibtex

@article{525ce661da5341589047e1e8926b5997,
title = "Endothelial Notch1 Activity Facilitates Metastasis",
abstract = "Endothelial cells (ECs) provide angiocrine factors orchestrating tumor progression. Here, we show that activated Notch1 receptors (N1ICD) are frequently observed in ECs of human carcinomas and melanoma, and in ECs of the pre-metastatic niche in mice. EC N1ICD expression in melanoma correlated with shorter progression-free survival. Sustained N1ICD activity induced EC senescence, expression of chemokines and the adhesion molecule VCAM1. This promoted neutrophil infiltration, tumor cell (TC) adhesion to the endothelium, intravasation, lung colonization, and postsurgical metastasis. Thus, sustained vascular Notch signaling facilitates metastasis by generating a senescent, pro-inflammatory endothelium. Consequently, treatment with Notch1 or VCAM1-blocking antibodies prevented Notch-driven metastasis, and genetic ablation of EC Notch signaling inhibited peritoneal neutrophil infiltration in an ovarian carcinoma mouse model.",
keywords = "Animals, Cell Movement, Cells, Cultured, Humans, Lung Neoplasms, Mice, Mice, Inbred C57BL, Neoplasm Invasiveness, Neoplasm Metastasis, Neutrophil Infiltration, Receptor, Notch1, Signal Transduction, Vascular Cell Adhesion Molecule-1, Journal Article",
author = "Elfriede Wieland and Juan Rodriguez-Vita and Liebler, {Sven S} and Carolin Mogler and Iris Moll and Herberich, {Stefanie E} and Elisa Espinet and Esther Herpel and Amitai Menuchin and Jenny Chang-Claude and Michael Hoffmeister and Christoffer Gebhardt and Hermann Brenner and Andreas Trumpp and Siebel, {Christian W} and Markus Hecker and Jochen Utikal and David Sprinzak and Andreas Fischer",
note = "Copyright {\textcopyright} 2017 Elsevier Inc. All rights reserved.",
year = "2017",
month = mar,
day = "13",
doi = "10.1016/j.ccell.2017.01.007",
language = "English",
volume = "31",
pages = "355--367",
journal = "CANCER CELL",
issn = "1535-6108",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Endothelial Notch1 Activity Facilitates Metastasis

AU - Wieland, Elfriede

AU - Rodriguez-Vita, Juan

AU - Liebler, Sven S

AU - Mogler, Carolin

AU - Moll, Iris

AU - Herberich, Stefanie E

AU - Espinet, Elisa

AU - Herpel, Esther

AU - Menuchin, Amitai

AU - Chang-Claude, Jenny

AU - Hoffmeister, Michael

AU - Gebhardt, Christoffer

AU - Brenner, Hermann

AU - Trumpp, Andreas

AU - Siebel, Christian W

AU - Hecker, Markus

AU - Utikal, Jochen

AU - Sprinzak, David

AU - Fischer, Andreas

N1 - Copyright © 2017 Elsevier Inc. All rights reserved.

PY - 2017/3/13

Y1 - 2017/3/13

N2 - Endothelial cells (ECs) provide angiocrine factors orchestrating tumor progression. Here, we show that activated Notch1 receptors (N1ICD) are frequently observed in ECs of human carcinomas and melanoma, and in ECs of the pre-metastatic niche in mice. EC N1ICD expression in melanoma correlated with shorter progression-free survival. Sustained N1ICD activity induced EC senescence, expression of chemokines and the adhesion molecule VCAM1. This promoted neutrophil infiltration, tumor cell (TC) adhesion to the endothelium, intravasation, lung colonization, and postsurgical metastasis. Thus, sustained vascular Notch signaling facilitates metastasis by generating a senescent, pro-inflammatory endothelium. Consequently, treatment with Notch1 or VCAM1-blocking antibodies prevented Notch-driven metastasis, and genetic ablation of EC Notch signaling inhibited peritoneal neutrophil infiltration in an ovarian carcinoma mouse model.

AB - Endothelial cells (ECs) provide angiocrine factors orchestrating tumor progression. Here, we show that activated Notch1 receptors (N1ICD) are frequently observed in ECs of human carcinomas and melanoma, and in ECs of the pre-metastatic niche in mice. EC N1ICD expression in melanoma correlated with shorter progression-free survival. Sustained N1ICD activity induced EC senescence, expression of chemokines and the adhesion molecule VCAM1. This promoted neutrophil infiltration, tumor cell (TC) adhesion to the endothelium, intravasation, lung colonization, and postsurgical metastasis. Thus, sustained vascular Notch signaling facilitates metastasis by generating a senescent, pro-inflammatory endothelium. Consequently, treatment with Notch1 or VCAM1-blocking antibodies prevented Notch-driven metastasis, and genetic ablation of EC Notch signaling inhibited peritoneal neutrophil infiltration in an ovarian carcinoma mouse model.

KW - Animals

KW - Cell Movement

KW - Cells, Cultured

KW - Humans

KW - Lung Neoplasms

KW - Mice

KW - Mice, Inbred C57BL

KW - Neoplasm Invasiveness

KW - Neoplasm Metastasis

KW - Neutrophil Infiltration

KW - Receptor, Notch1

KW - Signal Transduction

KW - Vascular Cell Adhesion Molecule-1

KW - Journal Article

U2 - 10.1016/j.ccell.2017.01.007

DO - 10.1016/j.ccell.2017.01.007

M3 - SCORING: Journal article

C2 - 28238683

VL - 31

SP - 355

EP - 367

JO - CANCER CELL

JF - CANCER CELL

SN - 1535-6108

IS - 3

ER -