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TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling

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TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling. / Becker, Christoph; Fantini, Massimo C; Schramm, Christoph; Lehr, Hans A; Wirtz, Stefan; Nikolaev, Alexei; Burg, Jürgen; Strand, Susanne; Kiesslich, Ralf; Huber, Samuel; Ito, Hiroaki; Nishimoto, Norihiro; Yoshizaki, Kazuyuki; Kishimoto, Tadamitsu; Galle, Peter R; Blessing, Manfred; Rose-John, Stefan; Neurath, Markus F.

in: IMMUNITY, Jahrgang 21, Nr. 4, 10.2004, S. 491-501.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Becker, C, Fantini, MC, Schramm, C, Lehr, HA, Wirtz, S, Nikolaev, A, Burg, J, Strand, S, Kiesslich, R, Huber, S, Ito, H, Nishimoto, N, Yoshizaki, K, Kishimoto, T, Galle, PR, Blessing, M, Rose-John, S & Neurath, MF 2004, 'TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling', IMMUNITY, Jg. 21, Nr. 4, S. 491-501. https://doi.org/10.1016/j.immuni.2004.07.020

APA

Becker, C., Fantini, M. C., Schramm, C., Lehr, H. A., Wirtz, S., Nikolaev, A., Burg, J., Strand, S., Kiesslich, R., Huber, S., Ito, H., Nishimoto, N., Yoshizaki, K., Kishimoto, T., Galle, P. R., Blessing, M., Rose-John, S., & Neurath, M. F. (2004). TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling. IMMUNITY, 21(4), 491-501. https://doi.org/10.1016/j.immuni.2004.07.020

Vancouver

Becker C, Fantini MC, Schramm C, Lehr HA, Wirtz S, Nikolaev A et al. TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling. IMMUNITY. 2004 Okt;21(4):491-501. https://doi.org/10.1016/j.immuni.2004.07.020

Bibtex

@article{eef0cfbf2aed4cb4976f8a4d317f41a5,
title = "TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling",
abstract = "Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-dependent IL-6 trans-signaling prevented tumor progression in vivo. Taken together, our data provide novel insights into TGF-beta signaling in colorectal cancer and suggest novel therapeutic approaches for colorectal cancer based on inhibition of TGF-beta-dependent IL-6 trans-signaling.",
keywords = "Animals, Blotting, Western, Colonic Neoplasms/immunology, DNA-Binding Proteins/immunology, Disease Models, Animal, Disease Progression, Endoscopy, Digestive System, Enzyme-Linked Immunosorbent Assay, Humans, Immunohistochemistry, Interleukin-6/immunology, Intestinal Mucosa/immunology, Mice, Mice, Knockout, Mice, Transgenic, Protein Serine-Threonine Kinases, Receptor, Transforming Growth Factor-beta Type II, Receptors, Interleukin-6/immunology, Receptors, Transforming Growth Factor beta/genetics, Recombinant Fusion Proteins/immunology, Reverse Transcriptase Polymerase Chain Reaction, STAT3 Transcription Factor, Signal Transduction/physiology, T-Lymphocytes/immunology, Trans-Activators/immunology, Transforming Growth Factor beta/genetics",
author = "Christoph Becker and Fantini, {Massimo C} and Christoph Schramm and Lehr, {Hans A} and Stefan Wirtz and Alexei Nikolaev and J{\"u}rgen Burg and Susanne Strand and Ralf Kiesslich and Samuel Huber and Hiroaki Ito and Norihiro Nishimoto and Kazuyuki Yoshizaki and Tadamitsu Kishimoto and Galle, {Peter R} and Manfred Blessing and Stefan Rose-John and Neurath, {Markus F}",
year = "2004",
month = oct,
doi = "10.1016/j.immuni.2004.07.020",
language = "English",
volume = "21",
pages = "491--501",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling

AU - Becker, Christoph

AU - Fantini, Massimo C

AU - Schramm, Christoph

AU - Lehr, Hans A

AU - Wirtz, Stefan

AU - Nikolaev, Alexei

AU - Burg, Jürgen

AU - Strand, Susanne

AU - Kiesslich, Ralf

AU - Huber, Samuel

AU - Ito, Hiroaki

AU - Nishimoto, Norihiro

AU - Yoshizaki, Kazuyuki

AU - Kishimoto, Tadamitsu

AU - Galle, Peter R

AU - Blessing, Manfred

AU - Rose-John, Stefan

AU - Neurath, Markus F

PY - 2004/10

Y1 - 2004/10

N2 - Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-dependent IL-6 trans-signaling prevented tumor progression in vivo. Taken together, our data provide novel insights into TGF-beta signaling in colorectal cancer and suggest novel therapeutic approaches for colorectal cancer based on inhibition of TGF-beta-dependent IL-6 trans-signaling.

AB - Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-dependent IL-6 trans-signaling prevented tumor progression in vivo. Taken together, our data provide novel insights into TGF-beta signaling in colorectal cancer and suggest novel therapeutic approaches for colorectal cancer based on inhibition of TGF-beta-dependent IL-6 trans-signaling.

KW - Animals

KW - Blotting, Western

KW - Colonic Neoplasms/immunology

KW - DNA-Binding Proteins/immunology

KW - Disease Models, Animal

KW - Disease Progression

KW - Endoscopy, Digestive System

KW - Enzyme-Linked Immunosorbent Assay

KW - Humans

KW - Immunohistochemistry

KW - Interleukin-6/immunology

KW - Intestinal Mucosa/immunology

KW - Mice

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Protein Serine-Threonine Kinases

KW - Receptor, Transforming Growth Factor-beta Type II

KW - Receptors, Interleukin-6/immunology

KW - Receptors, Transforming Growth Factor beta/genetics

KW - Recombinant Fusion Proteins/immunology

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - STAT3 Transcription Factor

KW - Signal Transduction/physiology

KW - T-Lymphocytes/immunology

KW - Trans-Activators/immunology

KW - Transforming Growth Factor beta/genetics

U2 - 10.1016/j.immuni.2004.07.020

DO - 10.1016/j.immuni.2004.07.020

M3 - SCORING: Journal article

C2 - 15485627

VL - 21

SP - 491

EP - 501

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 4

ER -