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. 2024 Nov 6;15(11):796. doi: 10.1038/s41419-024-07142-2

Fig. 7. OSMI-1 inhibits aggressive growth of NE transdifferentiated PCa cell in vitro and in vivo.

Fig. 7

A Cell viability assessed by CCK-8 assay treated with 20 μM OSMI-1 or an equivalent dose of DMSO at different time points in LNCaP-AI cells. B, C Representative images and quantification of EDU assay in indicated LNCaP-AI cells with 20 μM OSMI-1 or an equivalent dose of DMSO for 72 h. D, E Representative images and quantification of transwell migration and matrigel invasion assays in indicated LNCaP-AI cells. F–H Effect of OSMI-1 on tumorigenesis in vivo evaluated with xenografts model. LNCaP-AI cells were subcutaneously injected into nude mice and the nude mice were randomly divided into control (DMSO), OSMI-1 (1 mg/kg, intravenously) after 7 days. Each group was intravenously administered every other day for 4 weeks. Representative images of xenograft tumors(F), Tumor weight (G), The growth curve (H). I Proposed model for KIF1A in promoting development of NEPC. Increased KIF1A forms complex with OGT escaping ubiquitin-proteasome mediated degradation to enhance OGT stabilization and nucleus accumulation. Moreover, intranuclear OGT regulates OCT4 and β-catenin O-GlcNAcylation to promote EMT and stemness, ultimately facilitates NE transdifferentiation to NEPC induced by KIF1A.