Collectively, our findings indicated that PCa‐derived exosomes‐loaded NEAT1 upregulated RUNX2 to facilitate the osteogenesis of hBMSCs by competitively binding to miR‐205‐5p via the SFPQ/PTBP2 axis, therefore providing a potential therapeutic target to treat osteogenesis of hBMSCs in PCa. This evidence concerns the gene RUNX2 and posterior cortical atrophy.