Slc25a29, a member of the solute carrier family 25, is a mitochondrial transporter of basic amino acids, such as arginine, lysine, and homoarginine [3]. It plays a role in mitochondrial protein synthesis and amino acid degradation, and is involved in linking metabolic pathways occurring in the cytosol and mitochondrial matrix [3,4]. It is also associated with processes like the urea cycle and ornithine degradation pathway [4,6]. Genetic models, like knockout models, can be used to study its functions.

Knockout of SLC25A29 by Nuclease technology inhibited proliferation and migration of cancer cells both in vitro and in vivo, and led to an altered metabolic status with enhanced mitochondrial respiration and reduced glycolysis [2]. In lung adenocarcinoma, SLC25A29 was underexpressed and regulated endothelial cell phenotypes, with decreased expression leading to increased endothelial cell proliferation and migration and decreased apoptosis [1]. In prostate cancer, SLC25A29 is upregulated, correlating with metastatic features and serving as a high-risk prognostic factor, and may transactivate POLD1 via E2F1 [5]. In pancreatic cancer, the recruitment of numerous immune cells was negatively correlated with SLC25A29, and cisplatin sensitivity increased with its up-regulation [7].

In conclusion, Slc25a29 is essential for mitochondrial function and amino acid metabolism. Its knockout studies have revealed its significant roles in cancer-related processes such as cell proliferation, migration, metabolic regulation, and prognosis in various cancers including lung, prostate, and pancreatic cancers, providing insights into potential therapeutic strategies.