Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-

Philip M. Carpenter, Tetsuya Gatanaga, Hoa Nguyen, John C. Hiserodt

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

A potentially important tumor-host interaction is increased tumor-cell invasiveness in response to motility factors derived from stromal and lymphoid cells. Conditioned medium of IL-2-stimulated lymphocytes and fractions enriched in either T cells, natural killer (NK) cells, or monocytes induced motility in MCF-7 breast carcinoma cells. ELISA and antibody neutralization studies demonstrated that this effect was due to tumor necrosis factor-α (TNF-α) secretion by the lymphoid cells or the enriched fractions. Unstimulated leukocytes in direct contact with MCF-7 cells also induced motility that was inhibited by anti-TNF-α antiserum. Time-lapse video microscopy of cells exposed to 10 ng/ml TNF-α showed that motility was independent of its toxic effects. Immunoperoxidase showed that MCF-7 cells expressed both the 55-kDa and the 75-kDa TNF-α receptors (TNFR). Antiserum against the 55-kDa TNFR, like TNF-α, induced motility in MCF-7 cells. This was most likely due to cross-linking of the 55-kDa TNFR monomers, since the monomeric F(ab) did not produce this effect. Our results raise the possibility that TNF-α-induced motility is one mechanism by which tumor cells overcome the potential anti-tumor immune function of lymphocytes and macrophages in peri-tumoral infiltrates.

Original languageEnglish (US)
Pages (from-to)64-70
Number of pages7
JournalInternational Journal of Cancer
Volume71
Issue number1
DOIs
StatePublished - Apr 23 1997

Fingerprint

MCF-7 Cells
Monocytes
Tumor Necrosis Factor-alpha
Lymphocytes
Immune Sera
Neoplasms
Receptors, Tumor Necrosis Factor, Type II
Video Microscopy
Tumor Necrosis Factor Receptors
Poisons
Stromal Cells
Conditioned Culture Medium
Natural Killer Cells
Interleukin-2
Leukocytes
Enzyme-Linked Immunosorbent Assay
Macrophages
Breast Neoplasms
T-Lymphocytes
Antibodies

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-. / Carpenter, Philip M.; Gatanaga, Tetsuya; Nguyen, Hoa; Hiserodt, John C.

In: International Journal of Cancer, Vol. 71, No. 1, 23.04.1997, p. 64-70.

Research output: Contribution to journalArticle

Carpenter, Philip M. ; Gatanaga, Tetsuya ; Nguyen, Hoa ; Hiserodt, John C. / Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-. In: International Journal of Cancer. 1997 ; Vol. 71, No. 1. pp. 64-70.
@article{b67158db84624c3a93ae310c99c24cf9,
title = "Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-",
abstract = "A potentially important tumor-host interaction is increased tumor-cell invasiveness in response to motility factors derived from stromal and lymphoid cells. Conditioned medium of IL-2-stimulated lymphocytes and fractions enriched in either T cells, natural killer (NK) cells, or monocytes induced motility in MCF-7 breast carcinoma cells. ELISA and antibody neutralization studies demonstrated that this effect was due to tumor necrosis factor-α (TNF-α) secretion by the lymphoid cells or the enriched fractions. Unstimulated leukocytes in direct contact with MCF-7 cells also induced motility that was inhibited by anti-TNF-α antiserum. Time-lapse video microscopy of cells exposed to 10 ng/ml TNF-α showed that motility was independent of its toxic effects. Immunoperoxidase showed that MCF-7 cells expressed both the 55-kDa and the 75-kDa TNF-α receptors (TNFR). Antiserum against the 55-kDa TNFR, like TNF-α, induced motility in MCF-7 cells. This was most likely due to cross-linking of the 55-kDa TNFR monomers, since the monomeric F(ab) did not produce this effect. Our results raise the possibility that TNF-α-induced motility is one mechanism by which tumor cells overcome the potential anti-tumor immune function of lymphocytes and macrophages in peri-tumoral infiltrates.",
author = "Carpenter, {Philip M.} and Tetsuya Gatanaga and Hoa Nguyen and Hiserodt, {John C.}",
year = "1997",
month = "4",
day = "23",
doi = "10.1002/(SICI)1097-0215(19970328)71:1<64::AID-IJC12>3.0.CO;2-9",
language = "English (US)",
volume = "71",
pages = "64--70",
journal = "International Journal of Cancer",
issn = "0020-7136",
publisher = "Wiley-Liss Inc.",
number = "1",

}

TY - JOUR

T1 - Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-

AU - Carpenter, Philip M.

AU - Gatanaga, Tetsuya

AU - Nguyen, Hoa

AU - Hiserodt, John C.

PY - 1997/4/23

Y1 - 1997/4/23

N2 - A potentially important tumor-host interaction is increased tumor-cell invasiveness in response to motility factors derived from stromal and lymphoid cells. Conditioned medium of IL-2-stimulated lymphocytes and fractions enriched in either T cells, natural killer (NK) cells, or monocytes induced motility in MCF-7 breast carcinoma cells. ELISA and antibody neutralization studies demonstrated that this effect was due to tumor necrosis factor-α (TNF-α) secretion by the lymphoid cells or the enriched fractions. Unstimulated leukocytes in direct contact with MCF-7 cells also induced motility that was inhibited by anti-TNF-α antiserum. Time-lapse video microscopy of cells exposed to 10 ng/ml TNF-α showed that motility was independent of its toxic effects. Immunoperoxidase showed that MCF-7 cells expressed both the 55-kDa and the 75-kDa TNF-α receptors (TNFR). Antiserum against the 55-kDa TNFR, like TNF-α, induced motility in MCF-7 cells. This was most likely due to cross-linking of the 55-kDa TNFR monomers, since the monomeric F(ab) did not produce this effect. Our results raise the possibility that TNF-α-induced motility is one mechanism by which tumor cells overcome the potential anti-tumor immune function of lymphocytes and macrophages in peri-tumoral infiltrates.

AB - A potentially important tumor-host interaction is increased tumor-cell invasiveness in response to motility factors derived from stromal and lymphoid cells. Conditioned medium of IL-2-stimulated lymphocytes and fractions enriched in either T cells, natural killer (NK) cells, or monocytes induced motility in MCF-7 breast carcinoma cells. ELISA and antibody neutralization studies demonstrated that this effect was due to tumor necrosis factor-α (TNF-α) secretion by the lymphoid cells or the enriched fractions. Unstimulated leukocytes in direct contact with MCF-7 cells also induced motility that was inhibited by anti-TNF-α antiserum. Time-lapse video microscopy of cells exposed to 10 ng/ml TNF-α showed that motility was independent of its toxic effects. Immunoperoxidase showed that MCF-7 cells expressed both the 55-kDa and the 75-kDa TNF-α receptors (TNFR). Antiserum against the 55-kDa TNFR, like TNF-α, induced motility in MCF-7 cells. This was most likely due to cross-linking of the 55-kDa TNFR monomers, since the monomeric F(ab) did not produce this effect. Our results raise the possibility that TNF-α-induced motility is one mechanism by which tumor cells overcome the potential anti-tumor immune function of lymphocytes and macrophages in peri-tumoral infiltrates.

UR - http://www.scopus.com/inward/record.url?scp=0030936462&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030936462&partnerID=8YFLogxK

U2 - 10.1002/(SICI)1097-0215(19970328)71:1<64::AID-IJC12>3.0.CO;2-9

DO - 10.1002/(SICI)1097-0215(19970328)71:1<64::AID-IJC12>3.0.CO;2-9

M3 - Article

VL - 71

SP - 64

EP - 70

JO - International Journal of Cancer

JF - International Journal of Cancer

SN - 0020-7136

IS - 1

ER -