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Study of glutamine dependency for cell growth in pediatric cancer cells

Research Project

Project/Area Number 08672056
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 小児外科
Research InstitutionOsaka University

Principal Investigator

WASA Masafumi  Osaka University Medical School, Assistant Professor, 医学部, 助手 (10240467)

Co-Investigator(Kenkyū-buntansha) FUKUZAWA Masahiro  Osaka University Medical School, Associate Professor, 医学部, 助教授 (60165272)
OKADA Akira  Osaka University Medical School, Professor, 医学部, 教授 (40028569)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
KeywordsNeuroblastoma / Glutamine / Amino Acid Transport
Research Abstract

We examined the effects of glutamine deprivation on glutamine transport activity in human neuroblastoma. We used a human neuroblastoma cell line (SK-N-SH) for the study. In vitro cell growth was measured in medium containing two different glutamine concentrations (DMEM+1O%FBS+2 mM Glutamine (Control) and DMIEM+1O%FBS (Glutamine deprivation)). Plasma membrane glutamine transport was measured at 0, 8, 16 and 24 hours after glutamine deprivation and its kinetic characteristics (Km and Vmax) were determined. Data (mean SD) were analyzed and compaired with Student's t-test.
Glutamine transport occurred by the high affinity Na^+-dependent carrier (System ASC). CeLl growth rates were dependent on glutamine concentrations. Glutamine transport activity was significantly decreased at 8, 16, and 24 hours after glutamine deprivation. Kinetic studies demonstrated that glutamine deprivation decreased maximum transport velocity (Vmax) (Control, 13713 * 803 pmol/mg protein/mm ; Glutamine deprivation, 9553* 646, p< 0.01) without affecting transport affinity (Km).
Glutamine transport activity was decreased in glutamine-deprived human neuroblastoma by the mechanism of decreasing the number of System ASC glutamine transporter. This may diminish glutamine availability and thereby influence cell growth in glutamine-deprived cells.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] Masafumi Wasa: "Effect of Adaptation to Low Glutamine Concentrations on cancer Growth" Surgical Forum. 47. 538-541 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Kai Chen: "Insulin-Like Growth Factor-I Stimulates Intestinal Epithelial Cell Proliferation and Migration" Surgical Forum. 48. 716-718 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Masafumi Wasa.: "Effect of Adaptation to Low Glutamine concentrations on cancer Growth" Surgical Forum. 47. 538-541 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Kai Chen.: "Insulin-Like Growth Factor-1 Stimulates Intestinal Epithelial Cell Proliferation and Migration" Surgical Forum. 48. 716-718 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] 和佐 勝史: "Eflect of Adaptation to Low Glutamine Concentration S on Cawer Gruwth" Surgical Forum. 47. 538-541 (1996)

    • Related Report
      1997 Annual Research Report
  • [Publications] Kai Chen: "Insulin-Like Growth Factor-I Stimolateg Intestinal Epithelial Cell Prolileration and Migration" Surgical Forum. 48. 716-718 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] 和佐勝史: "Effect of Adaptation to Low Glutamine concentrations on Cancer Growth" Surgical Forum. 47. 538-541 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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