Metabolic Signaling Cascades Prompted by Glutaminolysis in Cancer

Abstract

Aberrant glutamatergic signaling has been implicated in altered metabolic activity and the demand to synthesize biomass in several types of cancer including melanoma. In the last decade, there has been a significant contribution to our understanding of metabolic pathways. An increasing number of studies are now emphasizing the importance of glutamate functioning as a signaling molecule and a building block for cancer progression. To that end, our group has previously illustrated the role of glutamatergic signaling mediated by metabotropic glutamate receptor 1 (GRM1) in neoplastic transformation of melanocytes in vitro and spontaneous development of metastatic melanoma in vivo. Glutamate, the natural ligand of GRM1, is one of the most abundant amino acids in humans and the predominant excitatory neurotransmitter in the central nervous system. Elevated levels of glutaminolytic mitochondrial tricarboxylic acid (TCA) cycle intermediates, especially glutamate, have been reported in numerous cancer cells. Herein, we highlight and critically review metabolic bottlenecks that are prevalent during tumor evolution along with therapeutic implications of limiting glutamate bioavailability in tumors.

Document Details

Document Type
Pub Defense Publication
Publication Date
Sep 14, 2020
Source ID
10.3390/cancers12092624

Entities

People

  • Raj Shah
  • Suzie Chen

Organizations

  • New Jersey Health Foundation
  • Small Business Innovation Research and Small Business Technology Transfer

Tags

Fields of Study

  • Biology
  • Chemistry

Readers

  • Molecular and Cellular Biology
  • Neuroscience
  • Oncology