Retinoblastoma

Scientists at Kyung-Hee University, College of Pharmacy describe research in leukemia cell biology

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"DNA flow cytometric analysis indicated that acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells. Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by acteoside, whereas the steady-state level of CDK4 was unaffected. The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after acteoside treatment in a time-dependent manner. In addition, acteoside markedly enhanced the binding of p21(CIP1/WAF1) and p27(KIP1) to CDK4 and CDK6, resulting in the reduction of CDK2, CDK4 and CDK6 activities. Moreover, the hypophosphorylated form of retinoblastoma increased, leading to the enhanced binding of protein retinoblastoma (pRb) and E2F1," wrote K.W. Lee and colleagues, Kyung-Hee University, College of Pharmacy.

The researchers concluded: "Our results further suggest that acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigenthe onset of acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities. These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of acteoside on human promyelocytic HL-60 cells."

Lee and colleagues published their study in Carcinogenesis (Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte. Carcinogenesis, 2007;28(9):1928-36).

For additional information, contact K.W. Lee, College of Pharmacy, Dept. of Pharmaceutical Biochemistry, Kyung-Hee University, Hoegi-Dong, Seoul 130-701, Korea.

The publisher's contact information for the journal Carcinogenesis is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England.

Keywords: Korea, Seoul, Leukemia Cell Biology, Carcinogenesis, Cell Biology, Enzyme Research, Hematology, Kinase, Leukemia, Oncology, Pharmaceuticals.

This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2007, Biotech Business Week via NewsRx.com.