Lymphocyte and monocyte-induced motility of MCF-7 cells by tumor necrosis factor-alpha
| Autor: | P M, Carpenter, T, Gatanaga, H P, Nguyen, J C, Hiserodt |
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| Rok vydání: | 1997 |
| Předmět: |
Microscopy
Video Dose-Response Relationship Drug Tumor Necrosis Factor-alpha Breast Neoplasms Immunohistochemistry Coculture Techniques Monocytes Receptors Tumor Necrosis Factor Cross-Linking Reagents Cell Movement Culture Media Conditioned Tumor Cells Cultured Humans Interleukin-2 Female Lymphocytes |
| Zdroj: | International journal of cancer. 71(1) |
| ISSN: | 0020-7136 |
| Popis: | 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-alpha (TNF-alpha) 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-alpha antiserum. Time-lapse video microscopy of cells exposed to 10 ng/ml TNF-alpha 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-alpha receptors (TNFR). Antiserum against the 55-kDa TNFR, like TNF-alpha, 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-alpha-induced motility is one mechanism by which tumor cells overcome the potential anti-tumor immune function of lymphocytes and macrophages in peri-tumoral infiltrates. |
| Databáze: | OpenAIRE |
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