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. 2022 Feb 25;29(9):1730–1743. doi: 10.1038/s41418-022-00960-x

Fig. 1. Overexpression of c-Myc in prostate cancer is due to both transcriptional and posttranslational regulation.

Fig. 1

A MYC is amplified in PrCa patients in TCGA database. B MYC amplification indicates worse prognosis of PrCa patients. C MYC amplification indicates higher mRNA levels of c-Myc oncoprotein. D MYC amplification does not indicate higher protein levels of c-Myc oncoprotein. E c-Myc protein abundance was not correlated with its mRNA levels in human PrCa samples in TCGA database. R = 0.02, p = 0.575. F SPOP mutation did not correlated with high c-Myc expression in human PrCa patients in TCGA. G–H Depletion of USP22, USP28, USP36 or USP37 did not change the protein level of c-Myc in 22Rv1 and C4-2 PrCa cells. 22Rv1 (G) and C4-2 (H) cells were infected lentivirus to deplete endogenous USP22, USP28, USP36 or USP37, and selected with puromycin for 72 h, and collected for immunoblot analysis. I Depletion of USP36, but not USP22, USP28 or USP37, compromised the tumorigenesis ability of PrCa cell lines. The PrCa cells (22Rv1, C4-2, DU145 and PC3) treated as in (G) and (H) were subjected to colony formation assay, and stained with crystal violet. The relevant raw data are provided in Supplementary Materials.