Effects of angiostatin on experimentally induced colon cancer in mice

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Angiogenesis is one of the steps in tumor growth, invasion and metastasis. Antiangiogenic therapy is supposed to be an attractive approach for antitumor treatment. Human plasminogen-derived angiostatin K1-3 is one of the most potent antiangiogenic agents currently known. However, it is unclear whether angiostatin has got protective effects on colon cancer formation. So we investigated the protective effects of angiostatin on tumor growth in experimental mouse model of colon tumorigenesis using 1,2-dimethylhydrazine (DMH) induction. Eight weeks old Balb/c mice were treated with subcutaneous DMH solution (20 mg/kg) once weekly throughout a period of 12 weeks. In angiostatin group, 6 weeks after the last DMH injection the animals were firstly treated with angiostatin (20μg/Mouse) intraperitoneally and then subcutaneously every 48 hours (5μg/Mouse) throughout a period of 12 weeks. During this time, phosphate buffered saline (PBS) was used for DMH group. The animals were killled at the eighteenth week after the last DMH injection. Histopathological lesions were classified as mild dysplasia, severe dysplasi and malign tumoral lesion. Both groups developed these lesions and mean numbers of mild dysplasia, severe dysplasia

and malign lesions were 2,28±1,79, 3.14±2,67 and 4,42±2,29 in DMH group and 2,71±1,38, 2,28±1,49 ve 3,71±2,29 in angiostatin group, respectively. Although in angiostatin group, there was a decrease in severe dysplasia and malign tumor lesions number compared with the DMH group, this decrease was not statistically significant (p>0.05). However there was an increase in mild dysplasia but it wasn’t significant (p>0.05). Our results show that angiostatin has got little protective effects in these doses but these effects are thought to be increased by using higher doses and systematic administration.

Tolga Ertekin
Farelerde deneysel olarak oluşturulan kolon kanseri üzerine angiostatin’in etkileri · 2008 · 97 sayfa.
Danışman: Doç. Dr. Nihat Ekinci

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