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Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome

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Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome. / Henry, L. A.; Johnson, D. A.; Sarrio, D.; Lee, S.; Quinlan, P.R.; Crook, T.; Thompson, A.M.; Reis-Filho, J. S.; Isacke, C. M.

In: Oncogene, Vol. 30, No. 9, 2011, p. 1046-1058.

Research output: Contribution to journalArticle

Harvard

Henry, LA, Johnson, DA, Sarrio, D, Lee, S, Quinlan, PR, Crook, T, Thompson, AM, Reis-Filho, JS & Isacke, CM 2011, 'Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome' Oncogene, vol 30, no. 9, pp. 1046-1058., 10.1038/onc.2010.488

APA

Henry, L. A., Johnson, D. A., Sarrio, D., Lee, S., Quinlan, P. R., Crook, T., ... Isacke, C. M. (2011). Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome. Oncogene, 30(9), 1046-1058. 10.1038/onc.2010.488

Vancouver

Henry LA, Johnson DA, Sarrio D, Lee S, Quinlan PR, Crook T et al. Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome. Oncogene. 2011;30(9):1046-1058. Available from: 10.1038/onc.2010.488

Author

Henry, L. A.; Johnson, D. A.; Sarrio, D.; Lee, S.; Quinlan, P.R.; Crook, T.; Thompson, A.M.; Reis-Filho, J. S.; Isacke, C. M. / Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome.

In: Oncogene, Vol. 30, No. 9, 2011, p. 1046-1058.

Research output: Contribution to journalArticle

Bibtex - Download

@article{fbe3fd9ad7d24500ad2471c87723c658,
title = "Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome",
keywords = "endoglin, CD105, breast cancer, TGF-beta, MCF10A, ErbB2, GROWTH-FACTOR-BETA, MOUSE SKIN CARCINOGENESIS, TGF-BETA, ENDOTHELIAL-CELLS, TRANSFORMING GROWTH-FACTOR-BETA-1, RECEPTOR, CANCER, MIGRATION, PROLIFERATION, ACTIVATION",
author = "Henry, {L. A.} and Johnson, {D. A.} and D. Sarrio and S. Lee and P.R. Quinlan and T. Crook and A.M. Thompson and Reis-Filho, {J. S.} and Isacke, {C. M.}",
year = "2011",
doi = "10.1038/onc.2010.488",
volume = "30",
number = "9",
pages = "1046--1058",
journal = "Oncogene",
issn = "0950-9232",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome

A1 - Henry,L. A.

A1 - Johnson,D. A.

A1 - Sarrio,D.

A1 - Lee,S.

A1 - Quinlan,P.R.

A1 - Crook,T.

A1 - Thompson,A.M.

A1 - Reis-Filho,J. S.

A1 - Isacke,C. M.

AU - Henry,L. A.

AU - Johnson,D. A.

AU - Sarrio,D.

AU - Lee,S.

AU - Quinlan,P.R.

AU - Crook,T.

AU - Thompson,A.M.

AU - Reis-Filho,J. S.

AU - Isacke,C. M.

PY - 2011

Y1 - 2011

N2 - <p>Tumor growth factor-beta (TGF-beta) signaling in cancer has been implicated in growth suppression of early lesions and enhancing tumor cell invasion and metastasis. However, the cellular mechanisms that determine this signaling output in individual tumors are still largely unknown. In endothelial cells, TGF-beta signaling is modulated by the TGF-beta co-receptor endoglin (CD105). Here we demonstrate that endoglin is expressed in a subset of invasive breast cancers and cell lines and is subject to epigenetic silencing by gene methylation. Endoglin downregulation in non-tumorigenic MCF10A breast cells leads to the formation of abnormal acini in 3D culture, but does not promote cell migration or transformation. In contrast, in the presence of activated ErbB2, endoglin downregulation in MCF10A cells leads to enhanced invasion into a 3D matrix. Consistent with these data, ectopic expression of endoglin in MDA-MB-231 cells blocks TGF-beta-enhanced cell motility and invasion and reduces lung colonization in an in vivo metastasis model. Unlike endothelial cells, endoglin does not modulate Smad-mediated TGF-beta signaling in breast cells but attenuates the cytoskeletal remodeling to impair cell migration and invasion. Importantly, in a large cohort of invasive breast cancers, lack of endoglin expression in the tumor cell compartment correlates with ENG gene methylation and poor clinical outcome. Oncogene (2011) 30, 1046-1058; doi:10.1038/onc.2010.488; published online 1 November 2010</p>

AB - <p>Tumor growth factor-beta (TGF-beta) signaling in cancer has been implicated in growth suppression of early lesions and enhancing tumor cell invasion and metastasis. However, the cellular mechanisms that determine this signaling output in individual tumors are still largely unknown. In endothelial cells, TGF-beta signaling is modulated by the TGF-beta co-receptor endoglin (CD105). Here we demonstrate that endoglin is expressed in a subset of invasive breast cancers and cell lines and is subject to epigenetic silencing by gene methylation. Endoglin downregulation in non-tumorigenic MCF10A breast cells leads to the formation of abnormal acini in 3D culture, but does not promote cell migration or transformation. In contrast, in the presence of activated ErbB2, endoglin downregulation in MCF10A cells leads to enhanced invasion into a 3D matrix. Consistent with these data, ectopic expression of endoglin in MDA-MB-231 cells blocks TGF-beta-enhanced cell motility and invasion and reduces lung colonization in an in vivo metastasis model. Unlike endothelial cells, endoglin does not modulate Smad-mediated TGF-beta signaling in breast cells but attenuates the cytoskeletal remodeling to impair cell migration and invasion. Importantly, in a large cohort of invasive breast cancers, lack of endoglin expression in the tumor cell compartment correlates with ENG gene methylation and poor clinical outcome. Oncogene (2011) 30, 1046-1058; doi:10.1038/onc.2010.488; published online 1 November 2010</p>

KW - endoglin

KW - CD105

KW - breast cancer

KW - TGF-beta

KW - MCF10A

KW - ErbB2

KW - GROWTH-FACTOR-BETA

KW - MOUSE SKIN CARCINOGENESIS

KW - TGF-BETA

KW - ENDOTHELIAL-CELLS

KW - TRANSFORMING GROWTH-FACTOR-BETA-1

KW - RECEPTOR

KW - CANCER

KW - MIGRATION

KW - PROLIFERATION

KW - ACTIVATION

U2 - 10.1038/onc.2010.488

DO - 10.1038/onc.2010.488

M1 - Article

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 9

VL - 30

SP - 1046

EP - 1058

ER -

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