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Glutamine promotes ovarian cancer cell proliferation through the mTOR/S6 pathway

Lingqin Yuan1, Xiugui Sheng2, Adam K Willson2

  • 1Department of Gynecologic OncologyShanDong Tumor Hospital and Cancer Institute, Jinan University, Jinan 250117, People's Republic of ChinaDivision of Gynecologic OncologyUniversity of North Carolina at Chapel Hill, CB #7572, Physicians Office Building Rm #B105, Chapel Hill, North Carolina 27599, USALineberger Comprehensive Cancer CenterUniversity of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA Department of Gynecologic OncologyShanDong Tumor Hospital and Cancer Institute, Jinan University, Jinan 250117, People's Republic of ChinaDivision of Gynecologic OncologyUniversity of North Carolina at Chapel Hill, CB #7572, Physicians Office Building Rm #B105, Chapel Hill, North Carolina 27599, USALineberger Comprehensive Cancer CenterUniversity of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Endocrine-Related Cancer
|June 6, 2015
PubMed

Insights

Targeting glutamine metabolism shows promise for ovarian cancer treatment. Glutamine fuels ovarian cancer cells, and inhibiting its metabolism reduces their proliferation and induces stress.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Glutamine is a key nutrient for tumor cell biosynthesis.
  • Targeting glutamine metabolism offers potential anti-tumorigenic strategies.
  • Ovarian cancer cell lines exhibit dependence on glutamine.

Purpose of the Study:

  • To investigate the effects of glutamine on ovarian cancer cell growth.
  • To analyze glutamine dependence in HEY, SKOV3, and IGROV-1 cell lines.
  • To explore the molecular mechanisms underlying glutamine's role in ovarian cancer.

Main Methods:

  • Assessing cytotoxicity, cell cycle, apoptosis, and cell stress.
  • Measuring glucose and glutamine metabolism.
  • Analyzing the modulation of mTOR/S6 and MAPK pathways.
  • Utilizing rapamycin to inhibit mTOR and siRNA to block S6 expression.

Main Results:

  • Glutamine administration dose-dependently increased proliferation in all tested ovarian cancer cell lines.
  • Glutamine depletion induced reactive oxygen species and endoplasmic reticulum stress.
  • Glutamine enhanced glutaminase (GLS) and glutamate dehydrogenase (GDH) activity via mTOR/S6 and MAPK pathways.
  • Inhibition of mTOR or S6 reduced GDH and GLS activity, decreasing proliferation.

Conclusions:

  • Glutamine metabolism is crucial for ovarian cancer cell proliferation.
  • Targeting glutamine metabolism pathways (mTOR, S6, MAPK) can inhibit cancer growth.
  • Inhibiting glutamine metabolism presents a potential therapeutic strategy for ovarian cancer.
Keywords:
glutamate dehydrogenaseglutaminasemTOR/S6ovarian cancersiRNA

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