Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 164, Issue 4, Pages 1183-1190Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63206-3
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Funding
- NCI NIH HHS [1R01 CA81209, R01 CA081209] Funding Source: Medline
- NIAID NIH HHS [1R01 AI35796, R01 AI035796] Funding Source: Medline
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Efforts to treat tumors have routinely depended on disruption of cell proliferation by a variety of methods, many involving stimulation of apoptosis. We have previously shown that a truncated form of 24-kd basic fibroblast growth factor consisting of the amino terminal 86 amino acids inhibits migration of tumor and endothelial cells in vitro. In the present study, this peptide was tested for its ability to suppress angiogenesis and tumor growth using the murine dorsal skin-fold chamber model in vivo. Treatment of MCF-7 breast carcinoma tumor spheroids with this peptide resulted in cessation of the angiogenic response and a significant reduction in tumor size. Blood vessels that did form were poorly developed. In addition to inhibiting angiogenesis, the peptide also inhibited migration of Lewis lung carcinoma cells away from the tumor core before onset of angiogenesis indicating that the peptide-mediated inhibition of migration affects both angiogenesis and tumor growth independently. Despite inhibition of tumor cell migration, the peptide had no effect on neutrophil or eosinophil chemotaxis. This study demonstrates that the truncated form of 24-kd basic fibroblast growth factor is effective in suppressing tumor development in vivo through inhibition of angiogenesis as well as inhibition of tumor cell migration without compromising other homeostatic events.
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