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. Author manuscript; available in PMC: 2019 Sep 26.
Published in final edited form as: Oncogene. 2019 Mar 26;38(26):5265–5280. doi: 10.1038/s41388-019-0791-9

Fig. 2.

Fig. 2

FDPS is differentially regulated in prostate adenocarcinoma and PTEN-deficient human and murine prostate cancer cells as compared to respective normal tissues/PTENWT counterparts. a-d FDPS mRNA and protein expression were screened in a panel of human and mouse prostate cancer cell lines differing by PTEN mutation/deletion status. Total RNA was isolated from indicated human and mouse normal and prostate cancer cells lines and subjected to semi-quantitative RT-PCR. a Relative fold change of FDPS expression in a normal immortalized prostate epithelial cell line and a panel of prostate cancer cell lines was normalized with the Ct value of GAPDH. The error bar represents the average of triplicate samples. b FDPS relative mRNA expression was analyzed by semi-quantitative RT-PCR in normal prostate-derived cells and PTEN cKO mouse-derived syngeneic cell lines. c, d Western blot analysis of FDPS and phosphorylated AKT expression in a panel of human and mouse prostate cancer cell lines. e Bar graph showing concordance of FDPS gene amplification and PTEN deletion/mutation status in same PCa cohorts using CBioportal. f Box plot shows a significant increase in the mean FDPS intensity in prostate adenocarcinoma tissues and PIN lesions compared to hyperplasia and normal prostate tissues (P<0.001). g-j Images represent FDPS immunohistochemical staining in prostate tissues, g normal prostate, h hyperplasia, i PIN and j prostate adenocarcinoma.