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Definition of molecular determinants of prostate cancer cell bone extravasation.

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Definition of molecular determinants of prostate cancer cell bone extravasation. / Barthel, Steven R; Hays, Danielle L; Yazawa, Erika M; Opperman, Matthew; Walley, Kempland C; Nimrichter, Leonardo; Burdick, Monica M; Gillard, Bryan M; Moser, Michael T; Pantel, Klaus; Foster, Barbara A; Pienta, Kenneth J; Dimitroff, Charles J.

in: CANCER RES, Jahrgang 73, Nr. 2, 2, 2013, S. 942-952.

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

Harvard

Barthel, SR, Hays, DL, Yazawa, EM, Opperman, M, Walley, KC, Nimrichter, L, Burdick, MM, Gillard, BM, Moser, MT, Pantel, K, Foster, BA, Pienta, KJ & Dimitroff, CJ 2013, 'Definition of molecular determinants of prostate cancer cell bone extravasation.', CANCER RES, Jg. 73, Nr. 2, 2, S. 942-952. <http://www.ncbi.nlm.nih.gov/pubmed/23149920?dopt=Citation>

APA

Barthel, S. R., Hays, D. L., Yazawa, E. M., Opperman, M., Walley, K. C., Nimrichter, L., Burdick, M. M., Gillard, B. M., Moser, M. T., Pantel, K., Foster, B. A., Pienta, K. J., & Dimitroff, C. J. (2013). Definition of molecular determinants of prostate cancer cell bone extravasation. CANCER RES, 73(2), 942-952. [2]. http://www.ncbi.nlm.nih.gov/pubmed/23149920?dopt=Citation

Vancouver

Barthel SR, Hays DL, Yazawa EM, Opperman M, Walley KC, Nimrichter L et al. Definition of molecular determinants of prostate cancer cell bone extravasation. CANCER RES. 2013;73(2):942-952. 2.

Bibtex

@article{a1c5212844c3422d841ed6fb3e086b5d,
title = "Definition of molecular determinants of prostate cancer cell bone extravasation.",
abstract = "Advanced prostate cancer commonly metastasizes to bone, but transit of malignant cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis. Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow, and prostate cancer cells exhibit firm adhesion to BMEC via ?1, ?4, and ?V?3 integrins in static assays. However, whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wise transendothelial migration into bone is not known. Here, we describe how metastatic prostate cancer cells breach BMEC monolayers in a step-wise fashion under physiologic hemodynamic flow. Prostate cancer cells tethered and rolled on BMEC and then firmly adhered to and traversed BMEC via sequential dependence on E-selectin ligands and ?1 and ?V?3 integrins. Expression analysis in human metastatic prostate cancer tissue revealed that ?1 was markedly upregulated compared with expression of other ? subunits. Prostate cancer cell breaching was regulated by Rac1 and Rap1 GTPases and, notably, did not require exogenous chemokines as ?1, ?V?3, Rac1, and Rap1 were constitutively active. In homing studies, prostate cancer cell trafficking to murine femurs was dependent on E-selectin ligand, ?1 integrin, and Rac1. Moreover, eliminating E-selectin ligand-synthesizing ?1,3 fucosyltransferases in transgenic adenoma of mouse prostate mice dramatically reduced prostate cancer incidence. These results unify the requirement for E-selectin ligands, ?1,3 fucosyltransferases, ?1 and ?V?3 integrins, and Rac/Rap1 GTPases in mediating prostate cancer cell homing and entry into bone and offer new insight into the role of ?1,3 fucosylation in prostate cancer development.",
keywords = "Animals, Humans, Male, Mice, Cell Movement, Cell Line, Tumor, Cell Adhesion, Bone Marrow Cells/metabolism, E-Selectin/metabolism, Prostatic Neoplasms/*pathology, Endothelium, Vascular/metabolism, Antigens, CD29/metabolism, Bone Neoplasms/*secondary, Integrin alphaVbeta3/metabolism, Animals, Humans, Male, Mice, Cell Movement, Cell Line, Tumor, Cell Adhesion, Bone Marrow Cells/metabolism, E-Selectin/metabolism, Prostatic Neoplasms/*pathology, Endothelium, Vascular/metabolism, Antigens, CD29/metabolism, Bone Neoplasms/*secondary, Integrin alphaVbeta3/metabolism",
author = "Barthel, {Steven R} and Hays, {Danielle L} and Yazawa, {Erika M} and Matthew Opperman and Walley, {Kempland C} and Leonardo Nimrichter and Burdick, {Monica M} and Gillard, {Bryan M} and Moser, {Michael T} and Klaus Pantel and Foster, {Barbara A} and Pienta, {Kenneth J} and Dimitroff, {Charles J}",
year = "2013",
language = "English",
volume = "73",
pages = "942--952",
journal = "CANCER RES",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Definition of molecular determinants of prostate cancer cell bone extravasation.

AU - Barthel, Steven R

AU - Hays, Danielle L

AU - Yazawa, Erika M

AU - Opperman, Matthew

AU - Walley, Kempland C

AU - Nimrichter, Leonardo

AU - Burdick, Monica M

AU - Gillard, Bryan M

AU - Moser, Michael T

AU - Pantel, Klaus

AU - Foster, Barbara A

AU - Pienta, Kenneth J

AU - Dimitroff, Charles J

PY - 2013

Y1 - 2013

N2 - Advanced prostate cancer commonly metastasizes to bone, but transit of malignant cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis. Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow, and prostate cancer cells exhibit firm adhesion to BMEC via ?1, ?4, and ?V?3 integrins in static assays. However, whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wise transendothelial migration into bone is not known. Here, we describe how metastatic prostate cancer cells breach BMEC monolayers in a step-wise fashion under physiologic hemodynamic flow. Prostate cancer cells tethered and rolled on BMEC and then firmly adhered to and traversed BMEC via sequential dependence on E-selectin ligands and ?1 and ?V?3 integrins. Expression analysis in human metastatic prostate cancer tissue revealed that ?1 was markedly upregulated compared with expression of other ? subunits. Prostate cancer cell breaching was regulated by Rac1 and Rap1 GTPases and, notably, did not require exogenous chemokines as ?1, ?V?3, Rac1, and Rap1 were constitutively active. In homing studies, prostate cancer cell trafficking to murine femurs was dependent on E-selectin ligand, ?1 integrin, and Rac1. Moreover, eliminating E-selectin ligand-synthesizing ?1,3 fucosyltransferases in transgenic adenoma of mouse prostate mice dramatically reduced prostate cancer incidence. These results unify the requirement for E-selectin ligands, ?1,3 fucosyltransferases, ?1 and ?V?3 integrins, and Rac/Rap1 GTPases in mediating prostate cancer cell homing and entry into bone and offer new insight into the role of ?1,3 fucosylation in prostate cancer development.

AB - Advanced prostate cancer commonly metastasizes to bone, but transit of malignant cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis. Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow, and prostate cancer cells exhibit firm adhesion to BMEC via ?1, ?4, and ?V?3 integrins in static assays. However, whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wise transendothelial migration into bone is not known. Here, we describe how metastatic prostate cancer cells breach BMEC monolayers in a step-wise fashion under physiologic hemodynamic flow. Prostate cancer cells tethered and rolled on BMEC and then firmly adhered to and traversed BMEC via sequential dependence on E-selectin ligands and ?1 and ?V?3 integrins. Expression analysis in human metastatic prostate cancer tissue revealed that ?1 was markedly upregulated compared with expression of other ? subunits. Prostate cancer cell breaching was regulated by Rac1 and Rap1 GTPases and, notably, did not require exogenous chemokines as ?1, ?V?3, Rac1, and Rap1 were constitutively active. In homing studies, prostate cancer cell trafficking to murine femurs was dependent on E-selectin ligand, ?1 integrin, and Rac1. Moreover, eliminating E-selectin ligand-synthesizing ?1,3 fucosyltransferases in transgenic adenoma of mouse prostate mice dramatically reduced prostate cancer incidence. These results unify the requirement for E-selectin ligands, ?1,3 fucosyltransferases, ?1 and ?V?3 integrins, and Rac/Rap1 GTPases in mediating prostate cancer cell homing and entry into bone and offer new insight into the role of ?1,3 fucosylation in prostate cancer development.

KW - Animals

KW - Humans

KW - Male

KW - Mice

KW - Cell Movement

KW - Cell Line, Tumor

KW - Cell Adhesion

KW - Bone Marrow Cells/metabolism

KW - E-Selectin/metabolism

KW - Prostatic Neoplasms/pathology

KW - Endothelium, Vascular/metabolism

KW - Antigens, CD29/metabolism

KW - Bone Neoplasms/secondary

KW - Integrin alphaVbeta3/metabolism

KW - Animals

KW - Humans

KW - Male

KW - Mice

KW - Cell Movement

KW - Cell Line, Tumor

KW - Cell Adhesion

KW - Bone Marrow Cells/metabolism

KW - E-Selectin/metabolism

KW - Prostatic Neoplasms/pathology

KW - Endothelium, Vascular/metabolism

KW - Antigens, CD29/metabolism

KW - Bone Neoplasms/secondary

KW - Integrin alphaVbeta3/metabolism

M3 - SCORING: Journal article

VL - 73

SP - 942

EP - 952

JO - CANCER RES

JF - CANCER RES

SN - 0008-5472

IS - 2

M1 - 2

ER -