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Differential gene expression in metastasizing cells shed from kidney tumors

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Differential gene expression in metastasizing cells shed from kidney tumors. / Bockhorn, Maximilian; Roberge, Sylvie; Sousa, Cristina; Jain, Rakesh K; Munn, Lance L.

in: CANCER RES, Jahrgang 64, Nr. 7, 01.04.2004, S. 2469-73.

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

Harvard

Bockhorn, M, Roberge, S, Sousa, C, Jain, RK & Munn, LL 2004, 'Differential gene expression in metastasizing cells shed from kidney tumors', CANCER RES, Jg. 64, Nr. 7, S. 2469-73.

APA

Bockhorn, M., Roberge, S., Sousa, C., Jain, R. K., & Munn, L. L. (2004). Differential gene expression in metastasizing cells shed from kidney tumors. CANCER RES, 64(7), 2469-73.

Vancouver

Bockhorn M, Roberge S, Sousa C, Jain RK, Munn LL. Differential gene expression in metastasizing cells shed from kidney tumors. CANCER RES. 2004 Apr 1;64(7):2469-73.

Bibtex

@article{45670f19c75a4b14a79f678b88b49638,
title = "Differential gene expression in metastasizing cells shed from kidney tumors",
abstract = "We developed a novel orthotopic mouse tumor model of renal cell carcinoma to collect and characterize cells spontaneously shed from SN12C (renal cell carcinoma) and SN12L1 (high metastatic variant of SN12C) tumors grown in kidneys of severe combined immunodeficient mice. Viability of the shed cell population was greater for SN12L1 tumors (25%) compared with SN12C tumors (11%, P < 0.05). Gene array analysis of 23 genes involved in metastasis showed that CD44, alpha3 integrin, and caveolin were down-regulated in the shed tumor cells compared with their primary counterparts, and blocking alpha3 integrin or CD44 function inhibited attachment and migration of both cell lines. These results suggest that cohesion of the cells within the primary tumor mediated by CD44 and alpha3 integrins hinders metastasis and that shedding is a passive process not necessarily mediated by cell migration in these tumors. Furthermore, resistance to apoptosis may enhance metastasis in the higher metastatic tumor.",
keywords = "Animals, Antigens, CD44, Apoptosis, Carcinoma, Renal Cell, Caveolin 1, Caveolins, Down-Regulation, Gene Expression Regulation, Neoplastic, Humans, Integrin alpha3, Kidney Neoplasms, Male, Mice, Mice, SCID, Neoplasm Metastasis, Neoplasm Transplantation, Transplantation, Heterologous",
author = "Maximilian Bockhorn and Sylvie Roberge and Cristina Sousa and Jain, {Rakesh K} and Munn, {Lance L}",
year = "2004",
month = apr,
day = "1",
language = "English",
volume = "64",
pages = "2469--73",
journal = "CANCER RES",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "7",

}

RIS

TY - JOUR

T1 - Differential gene expression in metastasizing cells shed from kidney tumors

AU - Bockhorn, Maximilian

AU - Roberge, Sylvie

AU - Sousa, Cristina

AU - Jain, Rakesh K

AU - Munn, Lance L

PY - 2004/4/1

Y1 - 2004/4/1

N2 - We developed a novel orthotopic mouse tumor model of renal cell carcinoma to collect and characterize cells spontaneously shed from SN12C (renal cell carcinoma) and SN12L1 (high metastatic variant of SN12C) tumors grown in kidneys of severe combined immunodeficient mice. Viability of the shed cell population was greater for SN12L1 tumors (25%) compared with SN12C tumors (11%, P < 0.05). Gene array analysis of 23 genes involved in metastasis showed that CD44, alpha3 integrin, and caveolin were down-regulated in the shed tumor cells compared with their primary counterparts, and blocking alpha3 integrin or CD44 function inhibited attachment and migration of both cell lines. These results suggest that cohesion of the cells within the primary tumor mediated by CD44 and alpha3 integrins hinders metastasis and that shedding is a passive process not necessarily mediated by cell migration in these tumors. Furthermore, resistance to apoptosis may enhance metastasis in the higher metastatic tumor.

AB - We developed a novel orthotopic mouse tumor model of renal cell carcinoma to collect and characterize cells spontaneously shed from SN12C (renal cell carcinoma) and SN12L1 (high metastatic variant of SN12C) tumors grown in kidneys of severe combined immunodeficient mice. Viability of the shed cell population was greater for SN12L1 tumors (25%) compared with SN12C tumors (11%, P < 0.05). Gene array analysis of 23 genes involved in metastasis showed that CD44, alpha3 integrin, and caveolin were down-regulated in the shed tumor cells compared with their primary counterparts, and blocking alpha3 integrin or CD44 function inhibited attachment and migration of both cell lines. These results suggest that cohesion of the cells within the primary tumor mediated by CD44 and alpha3 integrins hinders metastasis and that shedding is a passive process not necessarily mediated by cell migration in these tumors. Furthermore, resistance to apoptosis may enhance metastasis in the higher metastatic tumor.

KW - Animals

KW - Antigens, CD44

KW - Apoptosis

KW - Carcinoma, Renal Cell

KW - Caveolin 1

KW - Caveolins

KW - Down-Regulation

KW - Gene Expression Regulation, Neoplastic

KW - Humans

KW - Integrin alpha3

KW - Kidney Neoplasms

KW - Male

KW - Mice

KW - Mice, SCID

KW - Neoplasm Metastasis

KW - Neoplasm Transplantation

KW - Transplantation, Heterologous

M3 - SCORING: Journal article

C2 - 15059900

VL - 64

SP - 2469

EP - 2473

JO - CANCER RES

JF - CANCER RES

SN - 0008-5472

IS - 7

ER -