To investigate the role and mechanisms of SOAT1 gene expression in the development and progression of prostate cancer.

The expression of the SOAT1 gene was analyzed based on TCGA datasets and validated in prostate cancer cell lines. The correlation between SOAT1 gene expression and patient prognosis in prostate cancer was assessed through gene expression, methylation levels, and survival analysis. A gene knockout cell line was established using CRISPR-Cas9 technology, and gene expression levels were verified by Western blot. Cell proliferation and migration abilities were analyzed using MTS, colony formation, and transwell assays. The role and molecular mechanisms of SOAT1 in prostate cancer cells were further investigated through quantitative real-time polymerase chain reaction, Western blot, high-resolution mass spectrometry, and cellular energy metabolism experiments.

SOAT1 expression was upregulated in prostate cancer tissues (P<0.05), and high SOAT1 expression was associated with decreased patient survival. SOAT1 expression was not regulated by the androgen receptor signaling pathway and was unrelated to the process of acquired castration resistance (P>0.05). Knockout of SOAT1 inhibited prostate cancer cell proliferation by reducing mitochondrial metabolism (approximately 45% decrease in oxygen consumption and 55% reduction in production of adenosine triphosphate), independent of the androgen metabolic pathway.

Targeted knockout of SOAT1 can inhibit prostate cancer cell proliferation, epithelial-mesenchymal transition (EMT), and tumor stemness by reducing mitochondrial metabolism, suggesting its potential as a therapeutic target.