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KMID : 0545120030130040607
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Journal of Microbiology and Biotechnology
2003 Volume.13 No. 4 p.607 ~ p.612
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Inhibition of Cell-Cycle Progression in Human Promyelocytic Leukemia HL-60 Cells by MCS-C2, Novel Cyclin-Dependent Kinase Inhibitor
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KIM, MIN KYOUNG
CHO, YOUL-HEE/KIM, JUNG MOGG/CHUN, MOON WOO/LEE, SEUNG KI/LIM, YOONGHO/LEE, CHUL-HOON
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Abstract
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To elucidate the action mechanism of MCS-C2, a novel analogue of toyocamycin and sangivamycin. its effect on the expression of cell cycle-rebated proteins in the human myelocytic leukcmia cell line HL-60 was examined using Western blotting and a flow cytometric analysis. MCS-C2, a selective inhibitor of cyclin-dependent kinases. was found to inhibit cell growth in a time- and dose-dependent manner, and inhibits cell cycle progression by inducing the arrest at GI and G2/M phases, in HL-60 cells. The flow cytometric analysis revealed an appreciable arrest of cells in the G2/M phase of the cell cycle after treatment with MCS-C2. The HL-60 cell population increased gradually from 13% at 0 h, to 28% at 12 h in the G2/M phase. after exposure to 2 μM MCS-C2. Furthermore, Western blot analysis demonstrated that MCS-C2 induced the cell cycle arrest at GI phase through the inhibition of pRh phosphorylation. Hypophosphorylated pRb accumulated after treatment with 5 pM MCS-C2 for 12 h, whereas, the level of hyperphosphorylated pRh was reduced. Thus, treatment of the cell with MCS-C2 suppressed the hyperphosphorylated form of pRh with a commensurate increase in the hypophosphorylatcd form.
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