Abstract
Q-ing tumor glutaminase for therapy.
Highlights
Cancer cells reprogram metabolism to provide the energy, nucleotides, lipids, amino acids and other building blocks required to proliferate and survive in the stressful tumor microenvironment [1]
We found that LAP/ MYC hepatocellular carcinoma (HCC) tumors showed increased Gls expression and decreased Gls2 expression compared to surrounding tissue, and confirmed that the upregulation of GLS and downregulation of GLS2 is found in human HCC
Using a MYC-driven cell line as a model to study the effects of GLS inhibition, we demonstrated that BPTES treatment blocked DNA replication, resulting in cell death
Summary
Cancer cells reprogram metabolism to provide the energy, nucleotides, lipids, amino acids and other building blocks required to proliferate and survive in the stressful tumor microenvironment [1]. MYC-driven cell transformation induces dependence on extracellular glutamine and upregulates expression of SLC1A5 and GLS [1,2,3,4]. As GLS is broadly expressed in many cancer types and catalyzes the first step of glutamine catabolism, it represents a potential anti-cancer therapy target.
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