Abstract
The treatment of osteosarcoma patients exhibits individual variability, underscoring the critical importance of targeted therapy. Although (Solute carrier family 35 member A2) SLC35A2's role in the progression of various cancers has been extensively investigated, its specific implications in osteosarcoma remain unexplored. Leveraging data from the (The Cancer Genome Atlas) TCGA and (Genotype-Tissue Expression) GTEx databases, we have discerned that SLC35A2 is notably upregulated in osteosarcoma and correlates with the prognosis of osteosarcoma patients. Consequently, it becomes imperative to delve into the role of SLC35A2 in the context of osteosarcoma. Our research substantiates that SLC35A2 exerts a notable influence on mitochondrial autophagy in osteosarcoma, thereby exerting cascading effects on the proliferation, migration, invasion, and apoptosis of osteosarcoma cells. Mechanistically, SLC35A2 orchestrates mitochondrial autophagy via the PI3K/AKT/mTOR signaling pathway. Moreover, we have conducted rigorous animal experiments to further corroborate the repercussions of SLC35A2 on osteosarcoma growth. In summation, our study elucidates that SLC35A2's modulation of mitochondrial autophagy through the PI3K/AKT/mTOR signaling pathway constitutes a pivotal factor in the malignant progression of osteosarcoma, unveiling promising therapeutic targets for patients grappling with this condition.