ZNF384-regulated SLC31A1 expression promotes tumor proliferation and invasion in breast cancer.

SLC31A1, a copper transporter, has been implicated in copper metabolism processes. This study aims to explore the function and potential regulatory mechanisms of SLC31A1 in breast cancer. The TCGA database was utilized to analyze SLC31A1 expression across various cancer types. SLC31A1 expression in breast cancer tissues was validated in an independent cohort of 80 paired breast cancer and adjacent normal tissues. SLC31A1 expression was manipulated in MCF-7 and BT-549 breast cancer cells using shRNA and overexpression vectors. Cell proliferation, colony formation, and invasion assays were performed to assess the functional consequences of SLC31A1 manipulation. ZNF384, a potential transcription factor for SLC31A1, was identified through bioinformatics analysis, and its binding to the SLC31A1 promoter was confirmed using dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP). SLC31A1 expression was significantly elevated in breast cancer tissues, and high expression was associated with poor prognosis. SLC31A1 promoted cell viability, colony formation, and invasion. ZNF384 was identified as a transcription factor that regulates SLC31A1 expression, and its overexpression enhanced SLC31A1 expression, while knockdown of ZNF384 inhibited breast cancer cell proliferation and invasion. ChIP assays confirmed a direct interaction between ZNF384 and the SLC31A1 promoter. SLC31A1 plays a crucial role in the proliferation and invasion of breast cancer cells, and its expression is regulated by ZNF384. These findings highlight SLC31A1 as a potential therapeutic target and suggest that modulation of copper metabolism may offer novel strategies for breast cancer treatment.