Slc7a2, a cationic amino acid transporter, plays crucial roles in multiple biological processes. It is involved in amino acid-related metabolism, such as lysine and arginine metabolism, and is associated with pathways like the PI3K/Akt/NF-κB pathway [3]. It has significance in various physiological functions including cell proliferation and immune regulation [3,6]. Genetic models, especially knockout models, are valuable for studying its functions.

In cancer, loss-of-function studies have revealed diverse roles. In hepatocellular carcinoma, SLC7A2 deficiency promotes cancer progression by enhancing recruitment of myeloid-derived suppressor cells via upregulating CXCL1 through the PI3K/Akt/NF-κB pathway [3]. In ovarian cancer, knockdown of SLC7A2 promotes cell viability, invasion and migration [4]. In NSCLC, SLC7A2 silencing enhances cell proliferation and drug insensitivity while lower SLC7A2 expression is related to less immune infiltrates and worse prognosis [5]. In triple negative breast cancer, low SLC7A2 levels are associated with advanced stages and lymph node metastasis [2]. In glioblastoma stem cells, upregulation of SLC7A2 is part of a lysine catabolism reprogramming that impacts tumour immunity [1]. In pancreatic islets, Slc7a2 knockout mice show decreased arginine-stimulated glucagon and insulin secretion, indicating its role in islet hormone secretion [6].

In conclusion, Slc7a2 is essential for amino acid-related metabolism, cell proliferation, and immune regulation. Knockout mouse models have been instrumental in uncovering its roles in cancer development, progression, and islet function. Understanding Slc7a2 provides insights into disease mechanisms, potentially guiding the development of new therapeutic strategies for cancer and metabolic diseases.