Comment on 'Long noncoding RNA UCA1 promotes glutamine-driven anaplerosis of bladder cancer by interacting with hnRNP I/L to upregulate GPT2 expression' by Chen et al.'”

Abstract

Bladder cancer is prevalent cancer worldwide with poor outcomes for patients with high-grade disease. Emerging evidence shows that alteration of metabolic status drives tumorigenesis in bladder cancer. As long noncoding RNA urothelial cancer associated 1 (UCA1) is known to play an essential role in cancer metabolisms, such as glycolysis and glutaminolysis. Chen et al. report the novel function of UCA1 in glutamine metabolism through interacting with heterogeneous nuclear ribonucleoproteins (hnRNPs) I and L (hnRNP I/L). This study reveals that UCA1 promotes glutamic pyruvate transaminase 2 (GPT2) expression at the transcription level in mechanistic studies. Inhibition of either UCA1, hnRNPI/L, or GPT2 significantly reduces bladder cancer tumor growth in the mice model. This work explores a new mechanism for glutamine metabolism and the novel therapeutic target of the UCA1-hnRNPI/L-GPT2 axis across malignancies.