Inhibition of L-Type Amino Acid Transporter Modulates the Expression of Cell Cycle Regulatory Factors in KB Oral Cancer Cells

DOI Web Site Web Site PubMed 被引用文献14件 参考文献27件
  • Kim Chun Sung
    Department of Oralbiochemistry, Chosun University School of Dentistry
  • Moon In-Sung
    Oral Biology Research Institute, Chosun University School of Dentistry
  • Park Ju-Hyun
    Oral Biology Research Institute, Chosun University School of Dentistry
  • Shin Woo-Cheol
    Oral Biology Research Institute, Chosun University School of Dentistry
  • Chun Hong Sung
    Department of Biotechnology (BK21 Program), Chosun University
  • Lee Sook-Young
    Research Center for Oral Disease Regulation of the Aged, Chosun University School of Dentistry
  • Kook Joong-Ki
    Department of Oralbiochemistry, Chosun University School of Dentistry
  • Kim Heung-Joong
    Oral Biology Research Institute, Chosun University School of Dentistry
  • Park Joo-Cheol
    Department of Oral Histology and Developmental Biology, Seoul National University School of Dentistry
  • Endou Hitoshi
    Department of Pharmacology and Toxicology, Kyorin University School of Medicine
  • Kanai Yoshikatsu
    Department of Pharmacology, Osaka University Graduate School of Medicine
  • Lee Byung-Kwon
    Department of Microbiology, University of Tennessee
  • Kim Do Kyung
    Oral Biology Research Institute, Chosun University School of Dentistry

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The purpose of this study was to examine the effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), an inhibitor of L-type amino acid transporters, on the cell growth suppression in KB human oral cancer cells and to study the roles of cell cycle regulatory factors in the BCH-induced growth inhibition. The effect of BCH on cell growth suppression and the influence of BCH to cell cycle regulatory factors in KB cell growth inhibition were examined using cell cycle analysis, immunoblotting and immunoprecipitation. The BCH treatment induced cell cycle arrest at G1 phase in KB cells. The expression of cyclin D3 was remarkably decreased by BCH treatment. The BCH inhibited the expression of cyclin-dependent protein kinase 6 (CDK6) in a time-dependent manner. In addition, the expression of CDK inhibitor p27 was increased by BCH treatment in KB cells, but not CDK inhibitors p21 and p15. These results suggest that, in KB cells, the inhibition of LAT1 by BCH causes cell cycle arrest at G1 phase by inhibiting cyclin D3–CDK6 complex whereas increasing expression of a CDK inhibitor p27.

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