Abstract
Cancer metastasis involves distinct steps that depend on complicated tumor-host interactions. The hematogenous dissemination of tumor cells may be facilitated by factors that promote the arrest and adherence of cancer cells in capillaries. We examined whether anti-tumor monoclonal immunoglobulin M (IgM) antibodies promoted the hematogenous dissemination of B 16 melanoma cells in syngeneic mice. IgM monoclonal antibodies were generated that selectively bind to B 16 melanoma cells as compared to syngeneic fibroblasts, lymphocytes or Lewis lung carcinoma cells. Incubation of B16-BL6 or B 16-F0 melanoma cells with these IgM anti-tumor antibodies significantly increased the number of lung colonies as compared with control antibodies. Moreover, intraperitoneal injection of specific antibody also significantly increased lung colonization. All anti-tumor antibodies promoted the aggregation of B 16 melanoma cells. A chemically generated immunoglobulin G (IgG)-like fragment of an anti-tumor IgM antibody displayed greatly reduced tumor aggregation and, in contrast to intact IgM, did not significantly increase lung colonization of B16 melanoma cells. Neither intact IgM nor the IgG-like fragment enhanced the in vitro invasiveness of B 16 melanoma cells across Matrigel-coated membranes. Our results, therefore, suggest that besides their beneficial anti-tumor effects, anti-tumor IgM antibodies may also promote the hematogenous dissemination of cancer cells.
Original language | English |
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Pages (from-to) | 103-109 |
Number of pages | 7 |
Journal | Clinical and Experimental Metastasis |
Volume | 20 |
Issue number | 2 |
DOIs | |
State | Published - 14 Apr 2003 |
Keywords
- Aggregation
- IgM
- Melanoma
- Metastasis
- Monoclonal antibodies
- Tumor antigens