Targeting glutaminase and mTOR.

Kazuhiro Tanaka,Takashi Sasayama,Eiji Kohmura

doi:10.18632/oncotarget.5263

Abstract

Targeting glutaminase and mTOR.

Highlights

Comprehensive genomic and proteomic analyses demonstrate that there is nearly universal activation of the PI3K pathway in glioblastoma (GBM) patients [1]
We recently examined the role of glutamine metabolism in response to mTOR-targeted treatments for GBM [4]
MTOR-targeted treatments affected metabolic reprogramming and increased GLS expression to deliver glutamine carbon to the tricarboxylic acid (TCA) cycle, revealing that GBM cells were strongly addicted to glutamine

Summary

Introduction

Comprehensive genomic and proteomic analyses demonstrate that there is nearly universal activation of the PI3K pathway in glioblastoma (GBM) patients [1]. Oncogenic signaling pathways directly promote metabolic reprogramming to upregulate the biosynthesis of proteins, nucleotides, amino acids and lipids, required for the enhanced growth of cancer cells. These alterations include aerobic glycolysis known as the Warburg effect, which provides cancer cells selective advantages through enhanced catabolism of glutamine [3]. Cancer cells usually display persistent TCA cycle activity despite robust aerobic glycolysis and often require mitochondrial catabolism of glutamine to TCA cycle intermediates to maintain rapid proliferation.

Results

Conclusion