Belotecan hydrochloride, a synthetic and water-soluble camptothecin derivative, is inhibitor of topoisomerase I.
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Type I and type II topoisomerase inhibitors interfere with DNA ‘unwinding’ during DNA replication and RNA transcription. Topoisomerase I (TOP1) cuts one strand in the double-stranded DNA, independent of ATP. Belotecan HCl (CKD-602), the synthetic water-solube camptothecin analogue, a TOP1 inhibitor and has been shown to be effective in the treatment of various cancers. Treatment with belotecan showed a significant cytotoxic effect in all cervical cancer cell lines in a time- and dose-dependent manner. The IC50 values were 30 ng/ml for Caski cells, 150 ng/ml for HeLa cells, and 150 ng/ml for SiHa cells at 48h after treatment. A strong pro-apoptotic activity was observed in the treatment groups after 48 h of treatment. Compared to the control, apoptosis rates significantly increased in Caski, HeLa and Siha when treated with different concentrations (half the IC50 and IC50 values). The treatment increased the expression of PARP (Poly(ADP-ribose) polymerase), cleaved PARP and Bcl2-associated X protein (BAX). In addition, expression of both p53 and phosphorylated p53 (Ser15) was increased. Belotecan treatment induced the G2/M phase cell accumulation in all cell lines in a concentration-dependent manner. The protein expression levels of MMP2 and VEGF, two proteins known to be specifically related to the invasive ability of cells, decreased following belotecan treatment. In vivo, treatment with belotecan (25 mg/kg; intravenously) significantly inhibited the tumor growth of this xenograft model compared with the control (p < 0.05)[1].
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