Objective The present study aims to elucidate the molecular mechanisms underlying the association between solute carrier family 6 member 1 (SLC6A1) and the aggressive progression of prostate cancer, with a particular emphasis on its relationship with mitochondrial function. Methods To evaluate mitochondrial function, we detected mitochondrial membrane potential, adenosine triphosphate (ATP) production, intracellular reactive oxygen species (ROS) levels, and mitochondrial morphology in prostate cancer cell lines. Western blot was used to detect apoptosis‐related proteins. Gene set enrichment analysis (GSEA) was performed using The Cancer Genome Atlas (TCGA) prostate cancer dataset. Results Our findings indicated that silencing of SLC6A1 decreased mitochondrial membrane potential and ATP production while increasing intracellular ROS levels, accompanied by Bax upregulation and activation of the caspase pathway. Furthermore, GSEA results suggested that low SLC6A1 expression might trigger cell apoptosis via mitochondrial disruption mediated by the interaction between potassium and calcium channels. Conclusion These results highlighted the role of SLC6A1 in mitochondrial dysfunction associated with cell apoptosis in prostate cancer cells. This study has provided further insights into the molecular mechanisms of advanced prostate cancer and potential therapeutic targets.
Chen et al. (2026) studied this question.