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Start Over Author "Che XF" Journal cancer letters
2 results on '"Che XF"'

1. Down regulation of c-Myc and induction of an angiogenesis inhibitor, thrombospondin-1, by 5-FU in human colon cancer KM12C cells.

Author

Zhao HY, Ooyama A, Yamamoto M, Ikeda R, Haraguchi M, Tabata S, Furukawa T, Che XF, Iwashita K, Oka T, Fukushima M, Nakagawa M, Ono M, Kuwano M, and Akiyama S

Subjects
Cell Line, Tumor, Colonic Neoplasms genetics, Colonic Neoplasms pathology, Down-Regulation, Humans, MicroRNAs genetics, Multigene Family, Oligonucleotide Array Sequence Analysis, Angiogenesis Inhibitors genetics, Antimetabolites, Antineoplastic pharmacology, Colonic Neoplasms drug therapy, Fluorouracil pharmacology, Gene Expression Regulation, Neoplastic drug effects, Genes, myc, Promoter Regions, Genetic, Thrombospondin 1 genetics
Abstract

5-FU is commonly used for treatment of various solid tumors including colon carcinoma. We have previously demonstrated that Egr-1 induced by 5-FU enhanced TSP-1 expression in human colon cancer KM12C cells. In this study, a Genechip analysis of KM12C cells treated with 5-FU revealed down-regulation of 924 genes and up-regulation of 460 genes. The decreased expression of c-Myc mRNA and phosphorylated c-Myc were detected and confirmed by RT-PCR and immunoblotting. Since 5-FU induced the expression of TSP-1, we examined the effect of c-Myc on the TSP-1 promoter. Deletion of the TSP-1 promoter region in which binding sites for c-Myc reside had no effect on the TSP-1 promoter activity induced by 5-FU. Meanwhile, 5-FU dose-dependently decreased the expression of miR-17-92 cluster. These findings suggest that 5-FU decreased the expression of c-Myc and consequently miR-17-92 cluster and increased the expression of TSP-1 mRNA.

Published
2008
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2. Reversal of P-glycoprotein mediated multidrug resistance by a newly synthesized 1,4-benzothiazipine derivative, JTV-519.

Author

Che XF, Nakajima Y, Sumizawa T, Ikeda R, Ren XQ, Zheng CL, Mukai M, Furukawa T, Haraguchi M, Gao H, Sugimoto Y, and Akiyama S

Subjects
Antineoplastic Agents pharmacology, Benzamides, Cell Membrane, Cell Survival drug effects, Doxorubicin pharmacology, Flow Cytometry, Humans, Imatinib Mesylate, Immunoblotting, Multidrug Resistance-Associated Proteins metabolism, Piperazines pharmacology, Pyrimidines pharmacology, Tumor Cells, Cultured drug effects, Tumor Cells, Cultured metabolism, ATP Binding Cassette Transporter, Subfamily B, Member 1 metabolism, Drug Resistance, Multiple, Drug Resistance, Neoplasm, Thiazepines pharmacology
Abstract

A newly synthesized 1,4-benzothiazipine derivate, 4-[3-(4-benzylpiperidin-1-yl) propionyl]-7-methoxy-2,3,4,5-tetrahydro-1, 4-benzothiazepine monohydrochloride (JTV-519) was examined for its ability to reverse P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1) mediated multidrug resistance (MDR) in K562/MDR and KB/MRP cells, respectively. JTV-519 at 3 microM reversed the resistance of K562/MDR cells to vincristine (VCR), taxol, etoposide (VP16), adriamycin (ADM) and actinomycin D and at 0.5 or 1 microM reversed their resistance to STI571. JTV-519 at 10 microM enhanced the accumulation of ADM in K562/MDR cells to the level in parental K562 cells and inhibited the efflux of ADM from K562/MDR cells. Photoaffinity labeling of P-gp with 3H-azidopine was almost completely inhibited by 500 microM JTV-519. JTV-519 at 3 microM also partially reversed the resistance of KB/MRP cells to VCR and at 500 microM partially inhibited the photoaffinity labeling of MRP1 with (125)I-II-azidophenyl agosterol A (125I-azidoAG-A). These results suggest that JTV-519 reversed the resistance to the anti-cancer agents in P-gp and MRP1 overexpressing multidrug-resistant cells by directly binding to P-gp and MRP1, and competitively inhibiting transport of the anti-cancer agents.

Published
2002
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