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Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment.

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Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment. / Mueller, Lars; Goumas, Freya A; Affeldt, Marianne; Sandtner, Susanne; Gehling, Ursula; Brilloff, Silke; Walter, Jessica; Karnatz, Nadia; Lamszus, Katrin; Rogiers, Xavier; Bröring, Dieter.

In: AM J PATHOL, Vol. 171, No. 5, 5, 2007, p. 1608-1618.

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

Harvard

Mueller, L, Goumas, FA, Affeldt, M, Sandtner, S, Gehling, U, Brilloff, S, Walter, J, Karnatz, N, Lamszus, K, Rogiers, X & Bröring, D 2007, 'Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment.', AM J PATHOL, vol. 171, no. 5, 5, pp. 1608-1618. <http://www.ncbi.nlm.nih.gov/pubmed/17916596?dopt=Citation>

APA

Mueller, L., Goumas, F. A., Affeldt, M., Sandtner, S., Gehling, U., Brilloff, S., Walter, J., Karnatz, N., Lamszus, K., Rogiers, X., & Bröring, D. (2007). Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment. AM J PATHOL, 171(5), 1608-1618. [5]. http://www.ncbi.nlm.nih.gov/pubmed/17916596?dopt=Citation

Vancouver

Mueller L, Goumas FA, Affeldt M, Sandtner S, Gehling U, Brilloff S et al. Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment. AM J PATHOL. 2007;171(5):1608-1618. 5.

Bibtex

@article{6e439c297c19422398ae34aabb8dd383,
title = "Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment.",
abstract = "Cancer-associated stromal fibroblasts (CAFs) are the main cellular constituents of reactive stroma in primary and metastatic cancer. We analyzed phenotypical characteristics of CAFs from human colorectal liver metastases (CLMs) and their role in inflammation and cancer progression. CAFs displayed a vimentin(+), alpha-smooth-muscle actin(+), and Thy-1(+) phenotype similar to resident portal-located liver fibroblasts (LFs). We demonstrated that CLMs are inflammatory sites showing stromal expression of interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis. In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha). The effect of TNF-alpha on CAFs is inhibited by the nuclear factor-kappaB inhibitor parthenolide. Conditioned medium of CAFs and LFs similarly stimulated the migration of DLD-1, Colo-678, HuH7 carcinoma cells, and human umbilical vein endothelial cells in vitro. Pretreatment of CAFs with TNF-alpha increased the chemotaxis of Colo-678 colon carcinoma cells by conditioned medium of CAFs; however, blockage of IL-8 activity showed no inhibitory effect. In conclusion, these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target.",
author = "Lars Mueller and Goumas, {Freya A} and Marianne Affeldt and Susanne Sandtner and Ursula Gehling and Silke Brilloff and Jessica Walter and Nadia Karnatz and Katrin Lamszus and Xavier Rogiers and Dieter Br{\"o}ring",
year = "2007",
language = "Deutsch",
volume = "171",
pages = "1608--1618",
journal = "AM J PATHOL",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "5",

}

RIS

TY - JOUR

T1 - Stromal fibroblasts in colorectal liver metastases originate from resident fibroblasts and generate an inflammatory microenvironment.

AU - Mueller, Lars

AU - Goumas, Freya A

AU - Affeldt, Marianne

AU - Sandtner, Susanne

AU - Gehling, Ursula

AU - Brilloff, Silke

AU - Walter, Jessica

AU - Karnatz, Nadia

AU - Lamszus, Katrin

AU - Rogiers, Xavier

AU - Bröring, Dieter

PY - 2007

Y1 - 2007

N2 - Cancer-associated stromal fibroblasts (CAFs) are the main cellular constituents of reactive stroma in primary and metastatic cancer. We analyzed phenotypical characteristics of CAFs from human colorectal liver metastases (CLMs) and their role in inflammation and cancer progression. CAFs displayed a vimentin(+), alpha-smooth-muscle actin(+), and Thy-1(+) phenotype similar to resident portal-located liver fibroblasts (LFs). We demonstrated that CLMs are inflammatory sites showing stromal expression of interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis. In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha). The effect of TNF-alpha on CAFs is inhibited by the nuclear factor-kappaB inhibitor parthenolide. Conditioned medium of CAFs and LFs similarly stimulated the migration of DLD-1, Colo-678, HuH7 carcinoma cells, and human umbilical vein endothelial cells in vitro. Pretreatment of CAFs with TNF-alpha increased the chemotaxis of Colo-678 colon carcinoma cells by conditioned medium of CAFs; however, blockage of IL-8 activity showed no inhibitory effect. In conclusion, these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target.

AB - Cancer-associated stromal fibroblasts (CAFs) are the main cellular constituents of reactive stroma in primary and metastatic cancer. We analyzed phenotypical characteristics of CAFs from human colorectal liver metastases (CLMs) and their role in inflammation and cancer progression. CAFs displayed a vimentin(+), alpha-smooth-muscle actin(+), and Thy-1(+) phenotype similar to resident portal-located liver fibroblasts (LFs). We demonstrated that CLMs are inflammatory sites showing stromal expression of interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis. In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha). The effect of TNF-alpha on CAFs is inhibited by the nuclear factor-kappaB inhibitor parthenolide. Conditioned medium of CAFs and LFs similarly stimulated the migration of DLD-1, Colo-678, HuH7 carcinoma cells, and human umbilical vein endothelial cells in vitro. Pretreatment of CAFs with TNF-alpha increased the chemotaxis of Colo-678 colon carcinoma cells by conditioned medium of CAFs; however, blockage of IL-8 activity showed no inhibitory effect. In conclusion, these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target.

M3 - SCORING: Zeitschriftenaufsatz

VL - 171

SP - 1608

EP - 1618

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 5

M1 - 5

ER -