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. Author manuscript; available in PMC: 2019 Jun 19.
Published in final edited form as: Oncogene. 2018 Dec 19;38(16):2967–2983. doi: 10.1038/s41388-018-0608-2

Figure 1. Array analysis and genetically engineering mouse model identified that Met requires p19Arf in CRPC.

Figure 1.

(A) Microarray reanalysis identified that ARF regulates MET pathway. (B-D) IHC analysis of Met protein expression in mouse prostate tissues (B) or recurrent prostate tumors (C-D) In Pten/Trp53 mutant mice, p19Arf deletion decreases the recurrent growth of prostate tumors of castrated Pten/Trp53 mutant mice at 4–6 months of age (C). Data are indicated by individual dots with analysis of p value. Nuclear MET and nuclear β-Catenin expression decreases upon p19Arf deletion (D).