Antiproliferative activity of contragestazol (DL111-IT) in murine and human tumor models in vitro and in vivo.
PURPOSES: To evaluate the antiproliferative activity of contragestazol (DL111-IT) in vitro and in vivo and to elucidate potential molecular mechanisms. METHODS: Cell killing ability of DL111-IT was measured by MTT/Trypan blue exclusion method and murine and human tumor models; cell cycle was analyzed by flow cytometry; pRb, CDK4 and Cyclin D1 expressions were detected by western blotting. RESULTS: DL111-IT exhibited high efficiency on cell growth inhibition of 12 cancer cell lines, the IC50 values were 4.1-19.7 microg/ml. In Sarcoma-180 (S180) and Hepatoma-22 ( H22) tumor bearing mice models, the inhibition rates were 55.9 and 55.6%, respectively, at the doses of DL111-IT 12.5-50.0 mg/kg for 9 days consecutive administration. Human ovarian carcinoma (HO-8910) xenograft study showed that, nine administrations (within 15 days) of DL111-IT (12.5-50.0 mg/kg) significantly inhibited tumor growth with the inhibition rates ranging from 17.0 to 64.3%. DL111-IT induced G1 arrest and overexpression of pRb, CDK4 and Cyclin D1 were observed in HO-8910 cell line, suggesting that cell cycle regulation might contribute to the anticancer property of DL111-IT. CONCLUSIONS: DL111-IT could inhibit the proliferation of cancer cells both in vitro and in vivo via a cell cycle regulation pathway.[1]References
- Antiproliferative activity of contragestazol (DL111-IT) in murine and human tumor models in vitro and in vivo. Yang, B., He, Q.J., Zhu, D.Y., Lou, Y.J., Fang, R.Y. Cancer Chemother. Pharmacol. (2006) [Pubmed]
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