In silico analysis shows slc1a4 as a potential target of hsa-mir-133a for regulating glutamine metabolism in gastric cancer.

Cutting-edge research has spotlighted glutamine metabolism as a promising therapeutic target in managing gastric cancer. This investigation highlights the upregulated glutamine transporters by leveraging clinical data from the TCGA Database and the expression analysis of the transcriptome profile of stomach adenocarcinoma (STAD) patients. Notably, it identifies SLC1A4 as a potential glutamine transporter in STAD. The screening of human miRNAs conducted using the TargetScan database, and the subsequent docking analysis present multiple miRNAs with the potential of being explored as therapeutic agents. By integrating transcriptome profiling, miRNA screening, and molecular docking, this study reveals, for the first time, the potential of hsa-mir-133a-1 in targeting slc1a4, along with its known target mTOR, in stomach cancer. The myriad interactions that can be regulated by this silencing mechanism are anticipated to ultimately reduce glutamine uptake in STAD. This study provides compelling evidence of glutamine transport via SLC1A4 in stomach cancer and delves into how it might impact mTOR and some of its pivotal downstream molecules. Considering these findings, novel therapeutic strategies can be devised to further enhance existing methods for combating gastric cancer.