Accumulating evidence suggests that miRNAs perform a crucial role in the development of prostate cancer (PC); however, the role of miR-500 in Personal computer remains poorly recognized. the two main regulators in cell cycle, the protein manifestation of cyclinD1 and CDK2 were detected by western blot. The results showed that miR-500 inhibitor could significantly decrease the levels of cyclinD1 and CDK2, indicating that miR-500 plays an important part in the cell cycle redistribution in Personal computer-3 and LnCap cells. Luciferase assays recognized LRP1B as a direct target of miR-500, implicating miR-500 as an important mediator of cell proliferation in Personal computer. Finally, we showed that LRP1B manifestation was significantly down-regulated in Personal computer cells relative to matched adjacent non-tumor cells, showing that improved miR-500 manifestation may be the result of LRP1B inhibition in Personal computer. Emerging evidence suggests that miR-500 functions as either an oncogene or tumor suppressor depending on the type of malignancy [16]. These effects are highly dependent on its numerous manifestation levels in certain tumors, along with the function of target genes, including those regulating proliferation, invasion, and cell migration [17]. For example, Yamamoto, et al. reported that miR-500 is definitely abundantly indicated in the sera and tumor cells of hepatocellular carcinoma (HC) individuals, but could be restored to baseline levels following tumor resection [18]. Numerous studies have also suggested that ACP-196 distributor improved miR-500 manifestation may be associated with poor medical results in gastric tumors. In addition, miR-500 sustains nuclear factor-kappaB (NF-B) activation and induces gastric malignancy cell proliferation and resistance to apoptosis [17]. Despite these observations, the exact role, whether pro- or antimetastasis, of miR-500 in Personal computer remains poorly recognized. Here, we observed significant raises in miRNA-500 manifestation in Personal computer cells and cell lines, which may contribute to malignancy in Personal computer. To verify the hypothesis, Personal computer-3 and LnCap cells were transfected having ACP-196 distributor a miR-500 inhibitor, exposing potent suppression of proliferation in Personal computer-3 and LnCap cells. Taken collectively, these observations suggest that miR-500 is an important mediator of oncogenesis ACP-196 distributor in Personal computer. LRP1B, a member of the low denseness lipoprotein (LDL) receptor family, is identified as a new candidate tumor suppressor gene [19,20]. This gene takes on multiple tasks in normal cell function and development [21], probably mediated by its binding to extracellular ligands. This gene ACP-196 distributor has been found to be inactivated in various malignancies, including urothelial malignancy [22], esophageal carcinoma [23], ovarian malignancy [24], glioblastoma [25], gastric malignancy [26], thyroid malignancy [27], and lung carcinoma [28]. Although LRP1B has been identified as a tumor suppressor in several cancer types, its manifestation pattern and biological function in Personal computer remain poorly recognized. Here, we explored the manifestation, functions, and mechanism of action of LRP1B in Personal computer. Using a luciferase reporter assay, we showed that MKK6 LRP1B was a direct target of miR-500 in Personal computer. Moreover, miR-500 knockdown significantly enhanced LRP1B protein levels in Personal computer-3 and LnCap cells, while LRP1B overexpression markedly inhibited the proliferation in Personal computer-3 and LnCap cells, showing that LRP1B is an important downstream effector of miR-500 in Personal computer proliferation. Interestingly, our results showed the LRP1B levels were significantly reduced in Personal computer cells and cell lines, ACP-196 distributor indicating that down-regulation of LRP1B is at least partly due to improved miR-500 in Personal computer. In our study, we headed to a new target, which is definitely directly involved in many tumor developments. Exploring the specific and exact mechanism of miR-500 in prostate malignancy is useful for exact medical targetted therapy. However, more animal experiments and clinically relevant detections are required further study to determine miR-500 and LRP1B. In summary, we observed a strong down-regulation of miR-500 in Personal computer and demonstrated a role for miR-500 as an important mediator of cell proliferation and invasion in Personal computer. Our data show a suppressive part of miR-500 in Personal computer development and may be a predictive biomarker and a novel therapeutic target for patients with PC, and may improve the prognosis of patients. Abbreviations CDK2cyclin-dependent protein kinase2HChepatocellular carcinomaLDLlow density lipoproteinLRP1Blipoprotein receptor-related protein 1BNCnegative controlNF-Bnuclear factor-kappaBPCprostate cancerqRT-PCRquantitative real-time PCR Funding This work is usually supported by the National Natural Science Foundation of China [grant number 81703088]. Competing interests The author declares that there are no competing interests associated with the manuscript. Author contribution Z.Z.L., L.H. and L.J.L. designed the study. Z.Z.L., C.R., L.H. and L.J.L. collated the data, designed and developed the database, carried.