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  • Title: Increase of vinblastine accumulation by inhibitors of calmodulin-dependent cell functions in rat ascites hepatoma AH66 cells.
    Author: Wakusawa S, Takeda K, Miyamoto K, Hidaka H.
    Journal: Anticancer Res; 1992; 12(6B):2021-4. PubMed ID: 1363514.
    Abstract:
    ML-9, an inhibitor for myosin light chain kinase, and W-7, a calmodulin inhibitor, suppressed the efflux of vinblastine and increased the intracellular accumulation of vinblastine, but W-5, an inactive compound for calmodulin, did not so in rat ascites hepatoma AH66 cells, which have a multidrug-resistant phenotype. In sensitive counterpart AH66F cells, W-7 and ML-9 were less effective. W-7 and ML-9 did not interfere with [3H]azidopine photolabeling of P-glycoprotein in the plasma membrane from AH66 cells. While P-glycoprotein is reported to be superphosphorylated by protein kinases, W-7 did not influence the phosphorylation of the P-glycoprotein in AH66 cells. There may be an unknown Ca(2+)-calmodulin-dependent mechanism in the extrusion of vinblastine from AH66 cells.
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