CRISPR/Cas9 regulates EphA2-CDH1 axis to inhibit the migration of castration-resistant prostate cancer cells

We ued CRISPR/Cas9 to knock out EphA2 gene in PC3 cells, and overexpress EphA2 gene in Du145 cells with overexpressed plasmids to explore the underlying mechanisms of EphA2 function in castration-resistant prostate cancer(CRPC) and clinical relevance, providing more evidence for EphA2 as a potential therapeutic target for CRPC. Overall design: Comparative gene expression profiling analysis of RNA-seq data for PC3-EphA2-KO and control cells, DU145-EphA2-OE and control cells.