Reduced angiogenesis and tumor progression in gelatinase A-deficient mice.

Abstract

Matrix proteolysis is thought to play a crucial role in several stages of tumor progression, including angiogenesis, and the invasion and metastasis of tumor cells. We investigated the specific role of gelatinase A (matrix metalloproteinase 2) on these events using gelatinase A-deficient mice. In these mice, tumor-induced angiogenesis was suppressed according to dorsal air sac assay. When B16-BL6 melanoma cells or Lewis lung carcinoma cells were implanted intradermally, the tumor volumes at 3 weeks after implantation in the gelatinase A-deficient mice decreased by 39% for B16-BL6 melanoma and by 24% for Lewis lung carcinoma (P < 0.03 for each tumor). The number of lung colonies of i.v. injections fell by 54% for B16-BL6 melanoma and 77% for Lewis lung carcinoma (P < 0.014 and P < 0.0015, respectively). These results indicated that host-derived gelatinase A plays an important role in angiogenesis and tumor progression, suggesting the usefulness of gelatinase A inhibitors for anticancer chemotherapy.

• Authors: T Itoh, M Tanioka, H Yoshida, T Yoshioka, H Nishimoto, S Itohara
• Journal: Cancer research (Cancer Res) Vol. 58 Issue 5 Pg. 1048-51 (Mar 01 1998) ISSN: 0008-5472 [Print] United States
• PMID: 9500469 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Gelatinases
• Metalloendopeptidases
• Matrix Metalloproteinase 2

Topics

• Animals
• Cell Division
• Cell Movement (genetics)
• Gelatinases (deficiency, genetics)
• Humans
• Matrix Metalloproteinase 2
• Melanoma, Experimental (blood supply, genetics, pathology)
• Metalloendopeptidases (deficiency, genetics)
• Mice
• Mice, Mutant Strains
• Neovascularization, Pathologic (genetics)