Mesenchymal phenotype predisposes lung cancer cells to impaired proliferation and redox stress in response to glutaminase inhibition

Background Recent work has highlighted glutaminase (GLS) as a key player in cancer cell metabolism, providing glutaminederived carbon and nitrogen to pathways that support proliferation. There is significant interest in targeting GLS for cancer therapy however the gene is not frequently mutated or amplified in tumors. As a result, identification of tractable markers that predict GLS dependence is needed for translation of GLS inhibitors to the clinic.