Overexpression of FER1L4 decreased absorbance at OD 450?nM, indicating inhibition of cell proliferation in Personal computer-3 (c) and DU145 (d) cells. reduced prostate malignancy tissues than normal tissues. Higher manifestation of FER1L4 was associated with prostate malignancy cells of early stage (AJCC stage I/II). Overexpression of FER1L4 inhibited cell proliferation and advertised cell apoptosis in prostate malignancy cells. Bioinformatic analysis, RT-qPCR, RNA pull down assay and dual luciferase assay showed that FER1L4 upregulated F-box/WD repeat-containing protein 7 (FBXW7) tumor suppressor via sponging miR-92a-3p. Silencing of FBXW7 reversed the cell phenotypes caused by FER1L4 overexpression in prostate malignancy cells. Conclusion The data shown that FER1L4, a downregulated lncRNA in prostate malignancy, was pivotal for cell proliferation and survival of prostate malignancy. The study offered new sights into understanding of the LY 379268 signaling network in prostate malignancy and implied that FER1L4 might be a biomarker for individuals with prostate malignancy. Keywords: FER1L4, FBXW7, miR-92a-3p, Prostate malignancy, YAP1 signaling Background Prostate malignancy is the second most commonly diagnosed malignancy type for males, accounting for approximately 13.5% of newly diagnosed cancer cases in 2018 . A total of 359,000 individuals died from prostate malignancy yearly worldwide . The prognosis of individuals with prostate malignancy has been greatly improved with the development of system restorative approach including androgen deprivation, chemotherapy and surgery [2, 3]. However, the emergence of castration resistance and chemotherapy resistance limits the effectiveness of current treatment and threatened individuals lives [4, 5]. Therefore, finding of novel biomarkers and investigation of molecular mechanisms of prostate malignancy may provide insights for the analysis and treatment of prostate malignancy. Long non-coding RNAs (lncRNAs) are a class of endogenous non-coding RNAs with more than 200 nucleotides in length . Studies showed that lncRNAs could bind to RNA, DNA or protein to exert their biological functions [7, 8]. Relating to competing endogenous RNA (ceRNA) hypothesis , lncRNAs sponged miRNAs to compete their binding to target gene mRNA and controlled gene manifestation. Recent years, multiple studies exposed that lncRNA were implicated in malignancy pathogenesis and progression [10C12]. Large throughout sequencing shown that there were several differentially indicated lncRNAs between prostate tumors and normal cells . Many lncRNAs were identified as oncogenes or tumor suppressors in prostate malignancy [14, 15]. For example, lncRNA HOXD-AS1 was highly indicated in castration-resistant prostate malignancy and inhibited cell proliferation and chemotherapy resistance via recruiting WDR5 . LncRNA LY 379268 NEAT1 facilitated oncogene transcription by epigenetic changes of gene promoter in Personal computer-3 and VAaP cells . LncRNA MEG3 sponged miR-9-5p, upregulated QKI-5 and suppressed prostate malignancy cell proliferation, migration, invasion and induced apoptosis . Fer-1-like protein 4 LY 379268 (FER1L4) have recently captivated the researchers attention due to its involvement in the progression of malignancy [17, 18]. The biological part and molecular mechanism of FER1L4 in prostate malignancy is unfamiliar. F-box/WD repeat-containing protein 7 (Fbxw7) is frequently mutated in human being cancers of many types . Like a well-known F-box protein, FBXW7 is a component of E3 ligase complex, mediating the realizing and binding of complex to specific target proteins . Via focusing on oncogenes for degradation, FBXW7 functioned like a tumor suppressor to attenuate uncontrolled cell proliferation and induced cell apoptosis in malignancy cells [21C24]. LY 379268 In hepatocellular carcinoma, FBXW7 advertised cell apoptosis and ceased cell growth through focusing on YAP1 for degradation . In several malignancy types, downregulation of FBXW7 was responsible for elevation of c-Myc and malignancy progression [22C24]. FBXW7 also played a tumor suppressor part in prostate malignancy cells . The current study aimed to investigate the part of FER1L4 in prostate malignancy. The manifestation of FER1L4 was recognized in prostate tumors and matched normal tissues. The function part of FER1L4 was explored in prostate malignancy cells by cell proliferation and cell apoptosis assays. Bioinformatic analysis, RNA pull down assay, western blotting and dual luciferase reporter assay were applied to study the molecular mechanism of FER1L4 in prostate malignancy cells. Materials and methods Study subjects A total of 78 prostate tumors and adjacent normal tissues CACNA1G were from individuals with prostate malignancy during surgical removal of LY 379268 tumors in China-Japan Union hospital during July, 2015 to September, 2018. All individuals did not receive chemotherapy or radiotherapy before surgery. The individuals were aged 45C67 having a median age of 57.6??6.6. The tumors were staged as stage I.