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자료유형
학술저널
저자정보
Chairoungdua, Arthit (Department of Pharmacology and Toxicology, Kyorin University School of Medicine) Iribe, Yuji (Department of Pharmacology and Toxicology, Kyorin University School of Medicine) Kanai, Yoshikatsu (Department of Pharmacology and Toxicology, Kyorin University School of Medicine) Endou, Hitoshi (Department of Pharmacology and Toxicology, Kyorin University School of Medicine) Aisaki, Ken-ichi (Division of Cellular & Molecular Toxicology, National Institute of Health Sciences) Larashi, Katsuhide (Division of Cellular & Molecular Toxicology, National Institute of Health Sciences) Kanno, Jun (Division of Cellular & Molecular Toxicology, National Institute of Health Sciences) Baniasadi, Shadi (National Research Institute of Tuberculosis and Lung Diseases, Shaheed Beheshti University of Medical Science, Department of Pharmacology and Toxicology, Kyorin University School of M)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제30권 제4호
발행연도
2007.1
수록면
444 - 452 (9page)

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Inhibition of LAT1 (L-type amino acid transporter 1 ) activity in tumor cells could be effective in the inhibition of tumor cell growth by depriving tumor cells of essential amino acids. Because of the high level of expression of LAT1 in tumor cells, LAT1 inhibitors would be useful for anticancer therapy in suppressing tumor growth without affecting normal tissues. In recent years, cDNA microarray technique is useful technology for anticancer drug development. It allows identifying and characterizing new targets for developments in cancer drug therapy through the understanding genes involved in drug action. The present study was designed to investigate gene expression profile induced by LAT1 inhibitor using gene chip technology. Human bladder carcinoma cells (T24 cells) were treated with classical system L inhibitor 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH). Gene chip experiment was applied for treated and untreated cells after 3 and f2 h. Two independent experiments with a high degree of concordance identified the altered expression of 151 and 200 genes after 3 and 12 h BCH treatment. Among these genes, 132 and 13 were up-regulated and 19 and 187 were down-regulated by 3 and 12 h BCH treatment respectively. We found that BCH affected the expression of a large number of genes that are related to the control of cell survival and physiologic behaviors. These data are useful for understanding of intracellular signaling of cell growth inhibition induced by LAT1 inhibitors as candidate for anticancer drug therapy.

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