Betamethasone inhibits tumor development, microvessel density and prolongs survival in mice with a multiresistant adenocarcinoma TA3

• Published in: Biological research 2010, Vol.43 (3), p.317-322
• Main Authors: Garrido, Osvaldo, Letelier, René, Rosas, Carlos, Fuenzalida, Marcela, Ferreira, Arturo, Lemus, David
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - blood supply; Adenocarcinoma - drug therapy; angiogenesis; Angiogenesis Inhibitors - therapeutic use; Animals; Betamethasone - therapeutic use; betamethasone treatment; BIOLOGY; Drug Resistance, Multiple - drug effects; Drug Resistance, Neoplasm - drug effects; metastasis; Mice; Mice, Inbred A; Microvessels - drug effects; Neovascularization, Pathologic - drug therapy; Tumor Burden - drug effects; Tumor Cells, Cultured
• ISSN: 0716-9760; 0717-6287
• DOI: 10.4067/S0716-97602010000300008

Tumor resistance to traditional cancer treatments poses an important challenge to modern science. Thus, angiogenesis inhibition is an important emerging cancer treatment. Many drugs are tested and corticosteroids have shown interesting results. Herein we investigate the effect on microvessel density, survival time and tumoral volume of mice with TA3-MTX-R tumors. Twenty six mice were inoculated with l x l0⁶ tumor cells; 4-5 days after injection, six mice were injected with PBS (group A) and twenty mice were treated with β-met (group B). All animals from Group A died on day 22. Group B was divided into Bl (treated discontinued) and B2 (treated daily) and observed until day 88. All mice were processed for histo-immunohistochemical analysis and the blood vessels were counted. A decrease in microvessel density and tumoral volume and longer survival times were observed in the treated group. We propose that the antiangiogenic β-met effect explains, at least partially, its tumor inhibitory properties. As an important perspective, we will experimentally combine these strategies with those recently described by us with regard to the important antiangiogenic-antitumor effects of Trypanosoma cruzi calreticulin. Since the molecular targets of these strategies are most likely different, additive or synergic effects are envisaged.