SLC5A6 Regulates Lipid Metabolism and Lymph Node Metastasis in Cervical Cancer via FASN

The solute carrier protein SLC5A6 is associated with multiple malignant tumors, while its role in cervical cancer (CC) remains unexplored. This study aimed to investigate the expression pattern, biological functions, and underlying mechanisms of SLC5A6 in cervical cancer. It was found that the expression of SLC5A6 was significantly upregulated in cervical cancer tissues, and its high expression was associated with poorer overall survival of patients. In vitro functional experiments conducted in HeLa and SiHa cell lines demonstrated that overexpression of SLC5A6 enhanced cell proliferation, colony formation, and migration abilities, while inhibiting cell apoptosis; conversely, knockdown of SLC5A6 suppressed these oncogenic phenotypes. Further in vivo experiments confirmed that knockdown of SLC5A6 could inhibit the growth of xenograft tumors. Through transcriptomic analysis and pathway enrichment analysis, this study identified lipid metabolism as a key downstream pathway of SLC5A6, in which fatty acid synthase (FASN) serves as a crucial effector molecule. Mechanistically, SLC5A6 is responsible for the transmembrane transport of biotin. Reduced expression of SLC5A6 leads to a decrease in the expression of biotin-dependent acetyl-CoA carboxylase (ACC), which in turn downregulates its downstream target gene FASN. Importantly, knockdown of FASN could reverse the promotional effect of SLC5A6 overexpression on the growth of cervical cancer cells, indicating that SLC5A6 promotes cervical cancer progression through FASN-mediated reprogramming of lipid metabolism. In conclusion, this study identified SLC5A6 as a novel oncogenic factor in cervical cancer and reveals its mechanism of regulating lipid metabolism via FASN, suggesting that targeting the SLC5A6-FASN axis may serve as a potential therapeutic strategy for cervical cancer.