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Rapamycin Suppresses Tumor Growth and Alters the Metabolic Phenotype in T-Cell Lymphoma

Wasakorn Kittipongdaja1, Xuesong Wu1, Justine Garner1

  • 1Departments of Dermatology, Medical College of Wisconsin, Milwaukee, USA.

The Journal of Investigative Dermatology
|April 22, 2015
PubMed

Insights

Rapamycin combats T-cell lymphoma by inhibiting the mTOR pathway, reducing cancer cell glycolysis and glucose use. This metabolic shift counteracts the Warburg effect, suppressing tumor growth.

Area of Science:

  • Oncology
  • Cell Metabolism
  • Molecular Biology

Background:

  • The mechanistic target of rapamycin (mTOR) pathway regulates cell growth and metabolism.
  • Cancer cells exhibit altered metabolism, including increased glycolysis (Warburg effect), to meet high energy demands.
  • Targeting metabolic adaptations is a promising strategy for cancer therapy.

Purpose of the Study:

  • To investigate the anti-tumor effects of rapamycin in T-cell lymphoma models.
  • To characterize the metabolic changes induced by rapamycin in lymphoma cells.
  • To determine if rapamycin can counteract the Warburg effect in T-cell lymphoma.

Main Methods:

  • Utilized murine T-cell lymphoma (MBL2) and human cutaneous T-cell lymphoma (CTCL) cell lines (HH, Hut78).
  • Administered rapamycin in syngeneic or NSG mouse models of T-cell lymphoma.
  • Analyzed metabolic phenotypes, including glycolytic rate, glucose utilization, and gene expression of glucose transporters and glycolytic enzymes.
  • Assessed cell sensitivity to glucose deprivation and mitochondrial oxidative phosphorylation (OXPHOS) inhibition.

Main Results:

  • Rapamycin significantly suppressed T-cell lymphoma tumor growth in vivo.
  • Rapamycin treatment inhibited mTOR complex 1 and 2 (mTORC1/2).
  • Lymphoma cells treated with rapamycin showed reduced glycolytic rates and glucose uptake.
  • Expression of glucose transporters and glycolytic enzymes decreased in rapamycin-treated cells and tumors.
  • Rapamycin-treated cells exhibited reduced reliance on glycolysis and maintained sensitivity to OXPHOS inhibition.

Conclusions:

  • Rapamycin effectively suppresses T-cell lymphoma growth in preclinical models.
  • Rapamycin treatment shifts lymphoma cell metabolism away from aerobic glycolysis.
  • The findings demonstrate rapamycin's potential to counteract the Warburg effect in T-cell lymphoma.

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