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 language | English (US) |
|---|---|
| Pages (from-to) | 64-70 |
| Number of pages | 7 |
| Journal | International Journal of Cancer |
| Volume | 71 |
| Issue number | 1 |
| DOIs | |
| State | Published - Apr 23 1997 |
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ASJC Scopus subject areas
- Oncology
- Cancer Research
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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 journal › Article
}
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.
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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 -