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The Tumor Microenvironment02:17

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Cancer02:18

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Cell-programmed nutrient partitioning in the tumour microenvironment.

Bradley I Reinfeld1,2,3, Matthew Z Madden1,4, Melissa M Wolf2,3

  • 1Medical Scientist Training Program, Vanderbilt University, Nashville, TN, USA.

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|April 8, 2021
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Summary
This summary is machine-generated.

Immune cells and cancer cells preferentially consume different nutrients in the tumor microenvironment (TME). This cell-intrinsic nutrient partitioning, driven by mTORC1 signaling, impacts cancer immunity and could be targeted for therapies.

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Enrichment and Characterization of the Tumor Immune and Non-immune Microenvironments in Established Subcutaneous Murine Tumors
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Area of Science:

  • Cancer Biology
  • Immunology
  • Metabolism

Background:

  • Cancer cells utilize glucose via Warburg metabolism, forming the basis for Positron Emission Tomography (PET) imaging.
  • Tumor-infiltrating immune cells also depend on glucose, and their impaired metabolism in the tumor microenvironment (TME) can lead to immune evasion.
  • It remains unclear if immune cell metabolic dysregulation in the TME is due to intrinsic programs or nutrient competition with cancer cells.

Purpose of the Study:

  • To investigate the differential uptake and partitioning of glucose and glutamine by specific cell subsets within the TME.
  • To determine whether cell-intrinsic programs or nutrient availability dictates this metabolic dysregulation.
  • To explore the therapeutic and imaging potential of targeting cell-selective nutrient acquisition in the TME.

Main Methods:

  • Utilized Positron Emission Tomography (PET) tracers to quantify glucose and glutamine uptake in specific cell populations within the TME.
  • Analyzed nutrient partitioning across various cancer models, including myeloid cells, T cells, and cancer cells.
  • Investigated the role of mechanistic target of rapamycin complex 1 (mTORC1) signaling and gene expression in cell-intrinsic nutrient metabolism.

Main Results:

  • Myeloid cells exhibited the highest glucose uptake in the TME, followed by T cells and then cancer cells.
  • Cancer cells demonstrated the highest glutamine uptake compared to immune cells.
  • Cell-intrinsic programs, regulated by mTORC1 signaling, govern the preferential uptake of glucose and glutamine by immune and cancer cells, respectively.
  • Inhibition of glutamine uptake increased glucose uptake, indicating glutamine metabolism suppresses glucose utilization independently of glucose limitation.

Conclusions:

  • Cell-intrinsic programs dictate the distinct partitioning of glucose and glutamine between immune cells and cancer cells within the TME.
  • This selective nutrient acquisition influences immune cell function and cancer progression.
  • Targeting these cell-selective metabolic pathways offers potential for novel cancer therapies and advanced imaging strategies.