SLC7A5 serves as a potential therapeutic target for osteosarcoma: a comprehensive analysis based on bioinformatics and experimental validation.

This study aimed to investigate the role of solute carrier family 7 member 5 (SLC7A5) in osteosarcoma (OS) and its potential as a therapeutic target. Pan-cancer analysis revealed that SLC7A5 is significantly overexpressed in various tumor types, with particularly prominent upregulation in osteosarcoma. Using datasets from The Cancer Genome Atlas (TCGA), we found that high SLC7A5 expression was closely associated with poor patient prognosis, tumor multifocality, and metastatic progression. Based on SLC7A5-related genes, we constructed a prognostic risk score model using LASSO regression. This model effectively stratified patients by risk, revealing significant differences in survival outcomes between the high-risk and low-risk groups. In in vitro experiments, SLC7A5 overexpression significantly promoted the proliferation, migration, and invasion of osteosarcoma cells; conversely, silencing SLC7A5 not only inhibited these cellular behaviors but also induced apoptosis. Combining RNA sequencing with pathway enrichment analysis, we found that SLC7A5 regulates the phosphorylation levels of the mTOR pathway and its downstream target S6. In vivo experiments showed that SLC7A5 overexpression accelerated the growth of mouse xenograft tumors. Consistent with the in vitro functional assays, Ki-67 and phosphorylated mTOR levels were also elevated in tumor tissues, further validating the association between SLC7A5 and mTOR-mediated tumor progression.