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  • Title: Selective inhibition of the growth of ras-transformed human bronchial epithelial cells by emodin, a protein-tyrosine kinase inhibitor.
    Author: Chan TC, Chang CJ, Koonchanok NM, Geahlen RL.
    Journal: Biochem Biophys Res Commun; 1993 Jun 30; 193(3):1152-8. PubMed ID: 7686746.
    Abstract:
    Emodin (3-methyl-1,6,8-trihydroxyanthraquinone), a naturally occurring protein-tyrosine kinase inhibitor, selectively blocked the growth of v-ras-transformed human bronchial epithelial cells. Half-maximal inhibition of cell growth occurred at a concentration of 4 micrograms/ml. In contrast, emodin at a concentration of 100 micrograms/ml had little effect on the growth of normal human bronchial epithelial cells. Cell cycle analyses indicated that treatment with emodin arrested the v-ras-transformed cells in the G2/M phase of their cell cycle. Immunoblotting experiments using anti-phosphotyrosine antibodies indicated that ras-transformed cells, as compared to their normal counterparts, exhibited elevated levels of phosphotyrosine-containing proteins. Treatment with emodin resulted in a decrease in intracellular protein-tyrosine phosphorylation. These results suggest that compounds that inhibit the ras-dependent elevation in the level of tyrosine phosphorylated proteins may prove to be useful chemotherapeutic agents and may exhibit selective cytotoxicity against cancer cells with an activated ras oncogene.
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