Slc7a5, also known as LAT1, is an amino acid transporter that forms a heterodimeric complex with SLC3A2 (4F2hc) [4]. It is crucial for the efficient uptake of essential amino acids and hormones, promoting cellular growth by stimulating mTORC1 signalling and repressing the integrated stress response (ISR) [4].

Cancer cells highly express Slc7a5, and its high expression is linked to poor patient prognosis. Pharmacologic inhibition and knockdown/knockout of Slc7a5 suppress cancer cell proliferation and xenograft tumor growth [1]. In triple-negative breast cancer, knocking down Slc7a5 inhibits cell proliferation, migration, and invasion, and increases CD8+ T-cell infiltration [5]. In gastric cancer, circARID1A promotes cancer proliferation by forming a circARID1A-IGF2BP3-SLC7A5 RNA-protein ternary complex [2]. In lung cancer, IGF2BP2 enhances SLC7A5 mRNA stability and translation, and this positive feedback loop promotes radioresistance, while FBW7/GSK3β can degrade IGF2BP2 to inhibit this loop [3]. In systemic lupus erythematosus, SLC7A5 expression is up-regulated in peripheral blood T and B lymphocytes and is associated with renal damage [6]. In head and neck squamous cell carcinoma, TP63 transcriptionally regulates SLC7A5 to suppress ferroptosis [7]. In triple-negative breast cancer, the SLC7A5/E2F1/PTBP1/PKM2 axis mediates cancer progression and therapy effect through the crosstalk of amino acid metabolism and glycolysis pathway [8].

In conclusion, Slc7a5 is essential for amino acid uptake and cellular growth regulation. Model-based research, especially knockout/knockdown experiments, has revealed its significant roles in various diseases, particularly in cancer progression, immune-related diseases like systemic lupus erythematosus, and ferroptosis regulation in head and neck squamous cell carcinoma. Understanding Slc7a5 provides potential therapeutic targets for these diseases.