Fig. 5: NURR1 can function to enhance castration-resistant growth of prostate cancer cells in vivo. | Cell Death & Disease

Fig. 5: NURR1 can function to enhance castration-resistant growth of prostate cancer cells in vivo.

From: Nuclear receptor NURR1 functions to promote stemness and epithelial-mesenchymal transition in prostate cancer via its targeting of Wnt/β-catenin signaling pathway

Fig. 5

A, B In vivo tumorigenicity assay. A Images of dissected xenograft tumors grown in host mice (5-week post-castration) by VCaP-NURR1 and VCaP-vector infectants, and also VCaP-NURR1 infectants with IWP-2 treatment. B Semi-quantitative analysis of sizes of xenograft tumors grown in castrated mice by NURR1 Infectants with or without IWP-2 treatment. Results showed that in 28-day post-castration growth relapse, VCaP-NURR1 infectants grew tumors at faster rate than VCaP-vector infectants in castrated mice. However, treatment with IWP-2 could significantly suppress the castration-relapse tumor growth of VCaP-NURR1 infectants in castrated mice. C Immunoblot analyses of castration-relapse xenograft tumors formed by VCaP-NURR1 infectants. Results showed that castration-rebound VCaP-NURR1 tumors expressed higher levels of β-catenin and also enhanced levels of phenotypic markers of EMT (reduced E-cadherin and increased vimentin levels) and cancer stemness (increased CD44 and Oct4a, and decreased CD24 levels). However, expression levels of these phenotypic markers were either reduced or reversed upon treatment of host mice with IWP-2. **P < 0.01 VCaP-NURR1 versus VCaP-vector.

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