ETV4‑mediated transcriptional activation of SLC12A5 exacerbates ferroptosis resistance and glucose metabolism reprogramming in breast cancer cells

Solute carrier family 12 member 5 (SLC12A5) is an oncogene in numerous types of cancer, however its function in breast cancer (BC) remains elusive. ETS translocation variant 4 (ETV4) promotes BC. Therefore, the present study aimed to elucidate the role of SLC12A5 in ferroptosis and glucose metabolism in BC cells as well as to understand the underlying mechanism. Analysis of data from the UALCAN database demonstrated expression levels of SLC12A5 in BC and its association with prognosis. Reverse transcription‑quantitative PCR and western blotting were conducted to evaluate the expression levels of SLC12A5 and ETV4 in BC cells. The abilities of BC cells to proliferate, migrate and invade were assessed using Cell Counting Kit‑8, colony formation, wound healing and Transwell assays. Thiobarbituric acid reactive substances assay and a C11 BODIPY 581/591 probe were used to evaluate lipid peroxidation. Ferroptosis resistance was evaluated by the measurement of Fe