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PubMedDate not supplied

Concentration-dependent variable effects of etoposide on the cell cycle of CML cells.

BACKGROUND: Etoposide, a DNA-topoisomerase II inhibitor, is used for a broad spectrum of cancers with various therapeutic strategies. But the molecular mechanisms of its concentration-dependent effects are not clearly defined. MATERIALS AND METHODS: Chronic myelogenous leukemia K562 cells were treated with low (5 microM) or high (100 microM) concentrations of this drug and the changes of cell cycle progression, expression of cell cycle regulating genes and cyclin B1-dependent histone H1 kinase activity were studied. RESULTS: In the presence of 5 microM etoposide, K562 cells continued to synthesize DNA and most cells showed progress into G2 phase until 24 hours. In contrast, 100 microM etoposide rapidly inhibited DNA synthesis by around 6 hours and most cells remained in their initial phase, while the incorporation of bromodeoxyuridine was partially resumed from 12 hours. The histone H1 kinase activity was only down-regulated in the early phase of 100 microM treated cells. Among the cell cycle controlling genes, c-Myc and P21Cip1/WAF1 showed impressive responses to the two etoposide concentrations. At 100 microM, c-Myc protein rapidly vanished at 3 hours, while p21Cip1/WAF1 was inversely induced from 3 hours. These changes were also observed at 5 microM, but they occurred slowly and weakly. CONCLUSION: The present findings indicate that two concentrations of etoposide functioned as an anticancer agent through modulating the genes related in cell cycle progression. Differing responses of c-Myc and p21Cip1/WAF1 at two concentrations may govern the antiproliferative effects of etoposide.

Antineoplastic Agents, Phytogenic↗
PubMed2001

[Target therapy for CML--applying maxizyme].

Hammerhead type ribozyme, which have been frequently used for the purpose of specifically cleaving RNA at the GUC triplets in the experimental setting, can not be generally applicable for the gene therapy of leukemia with gene translocation. This is because the translocated sequence does not necessarily have the GUC triplets at the site of translocation. The introduction of new strategy which can specifically digest the chimera gene is considered to open new leukemia therapy with gene translocation. Maxizyme, a newly developed heterodimeric shortened ribozymes, can theoretically digest any types of chimeric genes at the site of translocation. In this review, our interesting results suggested the possible application of this maxizyme system for the treatment of chronic myelogenous leukemia with bcr/abl gene translocation.

Animals↗