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Lymphocyte and monocyte‐induced motility of MCF‐7 cells by tumor necrosis factor‐α
Author(s) -
Carpenter Philip M.,
Galanaga Tetsuya,
Nguyen Hoa P.,
Hiserodt John C.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970328)71:1<64::aid-ijc12>3.0.co;2-9
Subject(s) - motility , tumor necrosis factor alpha , biology , immune system , stromal cell , monocyte , cancer research , immunology , microbiology and biotechnology
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‐liking 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. Int. J. Cancer, 71:64–70, 1997. © 1997 Wiley‐Liss, Inc.