Ki-67 staining showed that, compared to that in the Lv-control group, the number of Ki-67-positive cells was higher in the Lv-SNHG17 group (< 0.05, Figures 3D,E). correlated with CD51 expression in prostate cancer. Mechanically, SNHG17 functioned as a competing endogenous RNA (ceRNA) to up-regulate CD51 expression through competitively sponging microRNA-144 (miR-144), and CD51 was identified as a direct downstream target of miR-144 in CRPC. Functionally, down-regulation of SNHG17 or up-regulation of miR-144 inhibited the proliferation, migration, and invasion of CRPC cells, whereas up-regulation of SNHG17 and down-regulation of miR-144 promoted the proliferation, migration and invasion of CRPC cells and formation and progression of bone metastases in CRPC by inhibiting EMT process and decreasing the prostate cancer stem cell population (pCSC) population (van der Horst et al., 2011). Interestingly, treatment with a humanized CD51 monoclonal antibody also showed excellent clinical benefit in some CRPC CI994 (Tacedinaline) patients with bone metastases in a multicenter phase I&II study (Wirth et al., 2014; Hussain et al., 2016). We also found CD51, which was down-regulated by p53 at transcriptional levels, was required for prostate cancer stemness and could enhance cancer initiation, metastatic potential, and chemoresistance (Sui et al., 2018). However, the regulation of CD51 in CRPC cells at the post-transcriptional levels remains unclear. In the current study, we showed that SNHG17 and miR-144 could regulate CD51 expression at post-transcriptional levels by functioning as ceRNA. Besides, CD51 was identified as the downstream effector and functional mediator of SNHG17 and miR-144 in CRPC. In addition, we found that SNHG17 promoted CRPC cell proliferation, migration and invasion and by targeting miR-144/CD51 axis. Hence, our study revealed the role of the SNHG17/miR-144/CD51 axis in accelerating CRPC cell proliferation and invasion, and suggested that SNHG17 may serve as a novel therapeutic target for CRPC. Materials and Methods Human Patient Samples Samples of 46 patients with CRPC and 149 patients with HSPC were provided by The First Affiliated Hospital of Xian Jiaotong University. The clinical-pathological features of prostate cancer patients enrolled in this study Slc4a1 were described in our previous study (Sui et al., 2018). Cell Culture Human prostate cancer cell lines LNCaP, C4-2, PC-3, and DU145 were purchased from GeneChem (Shanghai, China). LNCaP, DU145, CI994 (Tacedinaline) C4-2 and PC-3 cells were cultured in Dulbeccos modified eagle medium (DMEM, Gibco) containing 10% fetal bovine serum (FBS, Cellmax, Beijing, China), 1% penicillin-streptomycin (Cellmax) at 37C in a humidified atmosphere of 5% CO2. Construction of Lentivirus Expression Vector Lentiviral-SNHG17 (Lv-SNHG17), Lentiviral-CD51(Lv-CD51), and lentiviral scrambled negative control (Lv-control) were designed and provided by Genechem (Shanghai, China). Briefly, the full length of human SNHG17 (transcript variant 21), CD51 and scramble control were cloned intro Bam I and Kit (Ribo Bio) according to the manufacturers instructions. 105 cells were seeded in 96-well plates and stained with 100 L 50 CI994 (Tacedinaline) M EdU solution for 2 h in the dark at room temperature. Then, the cells were fixed with 4% paraformaldehyde for 30 min and permeabilized with 0.5% Triton X-100 for 15 min. After washing three times with PBS, the cells were stained with Apollo?567 and DAPI. Representative images were taken using the confocal microscope (Olympus, Japan) at 200 magnification. Wound Healing Assay, CCK-8, CI994 (Tacedinaline) Transwell Assay, and Western Blot (WB) Cell proliferation of different transfected PC-3 and C4-2 cells was further evaluated using CCK-8 assay. The migrative abilities of different transfected PC-3 and C4-2 cells were measured by wound healing assay. The invasive abilities of different transfected groups were measured by transwell assay. Protein.