7212079, No. significant differences in the expression of UAP1L1 in pathology grade, TFMB-(R)-2-HG Gleason score and Gleason grade (Table ?(Table2).2). Furthermore, Spearman correlation analysis TFMB-(R)-2-HG showed that this expression of UAP1L1 was positively correlated with pathology grade, Gleason score and Gleason grade, respectively (Table ?(Table3).3). Above all, UAP1L1 may be related to the process of prostate malignancy. Open in a separate window Fig. TFMB-(R)-2-HG 1 UAP1L1 upregulated in prostate malignancy tissues and promoted the proliferation and migration of prostate malignancy cells. A The expression levels of UAP1L1 was upregulated in prostate malignancy tissues, which was detected by immunohischemical staining. Magnification was 200 occasions and 400 occasions. B MTT assay results indicated that UAP1L1 knockdown inhibited the proliferation of prostate malignancy cells (DU 145 and PC-3). C The colony number in shUAP1L1 group was significantly decreased according to the results of clone formation assay. D The migration ability of prostate malignancy cells was determined by wound healing assay and the migration rate was reduced after UAP1L1 knockdown. E The invasion ability of prostate malignancy cells was detected through Transwell assay. ShCtrl: prostate malignancy cells infected with shRNA of control; shUAP1L1: prostate malignancy cells infected with shRNA of UAP1L1. **value 0.001 Table 2 Relationship between UAP1L1 expression and tumor characteristics in patients with prostate cancer TFMB-(R)-2-HG value 0.05,?** 0.01 Table 3 Relationship between UAP1L1 expression and tumor characteristics in patients with prostate malignancy 0.05,?** 0.01 UAP1L1 promoted human prostate cancer cell growth and inhibited cell apoptosis in vitro To explore the role of UAP1L1 in tumor growth, we used lentivirus targeting against UAP1L1 mRNA to suppress the expression of UAP1L1 in prostate cancer cell lines (DU 145 and PC3). The results showed that this lentivirus was efficiently transfected into DU 145 and PC3 cells (Additional file 1: Fig. S1A), and the qPCR analysis and WB assay recognized that the expression of UAP1L1 was significantly inhibited in both malignancy cells (Additional file 1: Fig. S1B, C). Subsequently, growth curve analysis showed that knockdown of UAP1L1 expression by lentivirus attenuated the growth of both prostate malignancy cells (Fig.?1B). Moreover, the capacity of cell proliferation was notably suppressed through the knockdown of UAP1L1 in both DU 145 and PC3 cells according to the results of colony formulation assay (Fig.?1C). Next, we further examined the impact of UAP1L1 knockdown on the capacity of invasion and migration, and cell apoptosis. The capacity of migration and invasion as characteristics of malignant cells was significantly suppressed by UAP1L1 knockdown in both DU 145 and PC3 cells (Fig.?1D and E). The results showed that this knockdown of UAP1L1 amazingly enhanced the apoptosis in both prostate malignancy cells (Fig.?2A). In the mean time, the analysis of Human Apoptosis Antibody Array indicated that after UAP1L1 knockdown in PC-3 cells, the expression levels of CD40L, IGFBP-3 and p21 was obviously upregulated (Fig.?2BCD). Altogether, these results indicated that UAP1L1 knockdown TFMB-(R)-2-HG inhibited prostate malignancy cell proliferation, invasion and migration in vitro, but induced cell apoptosis probably through regulating the expression of CD40L, IGFBP-3 and p21. Open in a separate windows Fig. 2 UAP1L1 knockdown inhibited the prostate malignancy cells apoptosis in vitro. A Circulation cytometry was used to detect the cell apoptosis, and the results indicated that shUAP1L1 inducted the apoptosis of prostate malignancy cells. B The intracellular signaling array after shUAP1L1 contamination was decided. The red box indicated upregulation of proteins expression. C The expression of proteins associated with cell apoptosis pathway in shUAP1L1 group LAMNB2 was compared to that in shCtrl group, and the fold switch was also offered. D The proteins with signaling changes in expression levels were shown in histograms. ShCtrl: prostate malignancy cells infected with shRNA of control; shUAP1L1: prostate malignancy cells infected with shRNA of UAP1L1. *exhibited that UAP1L1 was significantly upregulated in hepatocellular carcinoma tissues and UAP1L1 knockdown attenuated the growth of hepatocellular carcinoma cells [11]. Furthermore, studies decided that UAP1L1 knockdown inhibited the proliferation of glioma and esophageal squamous cell carcinoma cells and tumor growth in vivo [18, 19]. Similarly, the results of this study exhibited that UAP1L1 knockdown inhibited proliferation, clone formation ability, and migration of prostate malignancy cells (DU 145 and PC-3), and promoted the cell apoptosis. The apoptosis-related proteins (CD40L, IGFBP-3 and p21) were upregulated in the shUAP1L1 group in the Human Apoptosis Antibody Array analysis, suggesting that UAP1L1 knockdown might induced cell apoptosis via regulating the expression of CD40L, IGFBP-3.