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Fig. 1 | Molecular Cancer

Fig. 1

From: The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression

Fig. 1

PRMT5 is upregulated in PCa tissues and activates multiple signaling pathways. A Representative images of IHC staining of PRMT5 in PCa patients and their adjacent normal tissues. Scale bar: 50 μm. B Relative expression of PRMT5 levels (IHC score) in PCa tumor and paired adjacent normal tissues (n = 248). C and D Comparison of PRMT5 levels (H score) in different Gleason scores (GS) and T stages were analyzed in PCa samples (n = 248). E Kaplan–Meier curve was used to evaluate the progression-free survival (PFS) of PCa patients with high (n = 124) or low (n = 124) PRMT5 expression (Log-rank, P < 0.001). Data are shown as mean ± SD. *P < 0.05, **P < 0.01. F siRNA-mediated PRMT5 knockdown in PC-3 cells was confirmed by Western blot, and GAPDH was used as an internal control. G Phosphorylation of all screened proteins from PRMT5-depleted and control PC-3 cells based on a phosphospecific protein microarray analysis. H Among a total of 157 phosphorylation sites designed in the antibody array, phosphorylation at 67 sites was significantly altered (39 increased and 28 decreased) in PRMT5-depleted sample, compared with the control (fold-change PRMT5 KD vs. Control ≥ 1.2). I KEGG analysis of proteins in the phospho-specific protein microarray according to biological process, cellular component, molecular function. (Right panel) Heat map showing the fold change in expression of phosphorylated proteins in the PI3K-Akt pathway based on the phospho-specific protein microarray

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