The characteristics of androgen receptor splice variant 7 in the treatment of hormonal sensitive prostate cancer: a systematic review and meta-analysis.

BACKGROUND: Accumulating evidence suggests androgen receptor splice variant 7 (AR-V7) may be associated with the prognosis of castration-resistant prostate cancer (CRPC) received novel hormonal therapy while its characteristic and prognosis value in hormonal sensitive prostate cancer is unclear. METHODS: We aimed to evaluate the prognostic role of AR-V7 by progression free survival (PFS) and overall survival (OS) in hormonal sensitive prostate cancer (HSPC), and the AR-V7-positive-proportion difference in HSPC and CRPC. A search of PubMed, Embase, and the Web of Science was performed using the keywords prostate cancer, prostate tumor, prostate neoplasm, prostate carcinoma; AR-V7, AR3, androgen receptor splicing variant-7, or androgen receptor-3. Seventeen trials published due December 2019 were enrolled. RESULTS: AR-V7-positive proportion in CRPC was significantly larger than newly diagnosed prostate cancer (PCa) (odds ratio [OR] 7.06, 95% confidence interval [CI] 2.52-19.83, P < 0.001). Subgroup analyses indicated significantly higher AR-V7-positive proportion in CRPC derived from RNA in situ hybridization (OR 65.23, 95% CI 1.34-3171.43, P = 0.04), exosome RNA (OR 3.88, 95% CI 0.98-15.39, P = 0.05) and tissue RNA (OR 10.89, 95% CI 4.13-28.73, P < 0.001). AR-V7-positive patients had a significantly shorter PFS than those who were AR-V7-negative treated with first-line hormonal therapy (hazard ratio [HR] 3.63, 95% CI 1.85-7.10, P < 0.001) and prostatectomy (HR 2.49, 95% CI 1.33-4.64, P = 0.004). OS (HR 5.59, 95% CI 2.89-10.80, P < 0.001) were better in AR-V7-negative than AR-V7-positive HSPC patients treated with first-line hormonal therapy. The limitations of our meta-analysis were differences in study sample size and design, AR-V7 detection assay, and disease characteristics. CONCLUSION: AR-V7-positive proportion was significantly higher in CRPC than that in newly diagnosed PCa. AR-V7 positive HSPC patients portend worse prognosis of first-line hormonal therapy and prostatectomy. Additional studies are warranted to confirm these findings.

MiR-124 suppresses cell motility and adhesion by targeting talin 1 in prostate cancer cells.

BACKGROUND: MicroRNA is a type of endogenous non-coding RNA implicated in various cellular processes, and has been intensely investigated in the field of cancer research for many years. Here, we investigated the functions and mechanisms of miR-124 in prostate cancer, which is a putative tumor suppressor reported in many carcinomas. METHODS: Using bioinformatics, talin 1 was indicated as a potential target of miR-124. We examined the expression levels of miR-124 and talin 1 in tissue specimens and cell lines. To explore the relationship between miR-124 and talin 1, miR-124 mimics, miR-124 inhibitors, and talin 1 small interfering RNA (siRNA) were transiently transfected into cancer cell lines, followed by analysis using luciferase reporter assays. Next, to investigate the functions of miR-124 in prostate cancer, we performed cell attachment, migration, and invasion assays. A rescue experiment was also conducted to demonstrate whether miR-124 suppressed cell adhesion and motility by targeting talin 1. Finally, we examined the related signaling pathways of miR-124 and talin 1. RESULTS: MiR-124 was down-regulated in prostate cancer specimens and cell lines, while talin 1 was over-expressed in prostate cancer specimens and cell lines. These results showed an inverse correlation of miR-124 and talin 1 expression. Similar to talin 1 siRNA, overexpression of miR-124 by transient transfection of mimics led to a significant decrease in talin 1 levels. Luciferase report assays showed that the seed sequence of the talin 1 3'-untranslated region was a target of miR-124. Functional investigations revealed anti-attachment, anti-migration, and invasion-promoting effects of miR-124 in prostate cancer cells. The rescue experiment confirmed that miR-124 exerted its biological functions by targeting talin 1. Finally, we found that miR-124 and talin 1 impaired cellular adhesion and motility through integrins and the focal adhesion kinase/Akt pathway. CONCLUSIONS: Our study demonstrated biological roles and the related mechanism of miR-124 in prostate cancer. The results indicate that talin 1 is very likely a novel player in the anti-metastatic signaling network of miR-124. By down-regulation of talin 1, miR-124 impairs the adhesion, migration, and invasion of prostate cancer cells.

The iatrogenic injury of double vena cava due to misdiagnosis during the radical nephroureterectomy and cystectomy.

Double inferior vena cava (d-IVC) is a subtype of vascular anomaly that rarely needs treatment. Here, we present a rare case of d-IVC accompanied with concurrent renal pelvis and bladder carcinoma. Due to misdiagnosis, the anomalous left inferior vena cava (IVC) entering the left renal vein was mistaken as the gonadal vein and was then severed during the radical nephroureterectomy. Fortunately, the injured left IVC was recognized correctly during the following cystectomy. The vascular reconstruction operation was performed to recanalize the left iliac veins by anastomosing the ligated vascular stump to the right IVC in an 'end-to-side' way. During the hospitalization, the patient was treated with 'low molecular weight heparin' and then warfarin to ensure an ideal international normalized ratio. He recovered well from the surgery. A meticulous and comprehensive analysis of radiographic imaging is critical to avoid misdiagnosis of d-IVC.

Downregulation of microRNA-182-5p contributes to renal cell carcinoma proliferation via activating the AKT/FOXO3a signaling pathway.

BACKGROUND: Emerging evidence has suggested that dysregulation of miR-182-5p may contribute to tumor development and progression in several types of human cancers. However, its role in renal cell carcinoma (RCC) is still unknown. METHODS: Quantitative RT-PCR was used to quantify miR-182-5p expression in RCC clinical tissues. Bisulfite sequencing PCR was used for DNA methylation analysis. The CCK-8, colony formation, flow cytometry, and a xenograft model were performed. Immunohistochemistry was conducted using the peroxidase and DAB methods. A miR-182-5p target was determined by luciferase reporter assays, quantitative RT-PCR, and Western blotting. RESULTS: miR-182-5p is frequently down-regulated in human RCC tissues. Epigenetic modulation may be involved in the regulation of miR-182-5p expression. Enforced expression of miR-182-5p in RCC cells significantly inhibited the proliferation and tumorigenicity in vitro and in vivo. Additionally, overexpression of miR-182-5p induced G1-phase arrest via inhibition of AKT/FOXO3a signaling. Moreover, FLOT1 was confirmed as a target of miR-182-5p. Silencing FLOT1 by small interfering RNAs phenocopied the effects of miR-182-5p overexpression, whereas restoration of FLOT1 in miR-182-5p -overexpressed RCC cells partly reversed the suppressive effects of miR-182-5p. CONCLUSIONS: These findings highlight an important role for miR-182-5p in the pathogenesis of RCC, and restoration of miR-182-5p could be considered as a potential therapeutic strategy for RCC therapy.

Primary ectopic atypical meningioma in the renal hilum: a case report.

BACKGROUND: Primary ectopic atypical meningioma involving the renal hilum is rare. This is, to our knowledge, only the second case report of a primary retroperitoneal meningioma and the first case of an atypical subtype in this location. CASE PRESENTATION: A 53-year-old Han Chinese man presented with a 2-year history of left-side flank pain. An oval-shaped retroperitoneal mass was found in the left renal hilum on computed tomography, which was resected en bloc along with the kidney via laparotomy. According to the World Health Organization criteria, the tumor was histopathologically classified as a meningioma (Grade II, atypical). Five years later, the tumor recurred at the primary site with a similar histopathology. The patient received palliative resection, followed by radiotherapy (4500 cGy in 25 fractions). No relapse was found at 6-month follow-up. CONCLUSION: We describe the clinical, radiographic and histopathological features of an unusual case of aggressive ectopic meningioma in the renal hilum. The patient presented with a massive retroperitoneal tumor without primary cerebral or secondary metastatic lesions; the preoperative diagnosis was naturally confined to the common retroperitoneal malignancies. This case is of interest to oncologists, because of both its rare location and aggressiveness; it not only enriched the spectrum of primary ectopic meningioma, but also reminded us of potential recurrence of an atypical meningioma. This case raises the issue of the etiology of such a rare tumor that needs further investigation, and more importantly demands long-term follow-up result.

MicroRNA-101 suppresses motility of bladder cancer cells by targeting c-Met.

MicroRNAs (miRNAs) are small non-coding RNAs that play regulatory roles by repressing translation or cleaving RNA transcripts. Here, we report that the expression of microRNA-101 (miR-101) is down-regulated in human bladder cancer tissue versus normal adjacent tissue. To better characterize the role of miR-101 in bladder cancer, we conducted a gain-of-function analysis by transfecting the bladder cancer cell line T24 with chemically synthesized miR-101 mimics. We found that miR-101 directly targets c-Met via its 3'-UTR. Specifically, forced expression of miR-101 decreased c-Met expression at both mRNA and protein levels, consequently inhibiting T24 cell migration and invasion in a c-Met-dependent manner. In conclusion, we have shown miR-101 to be a novel suppressor of T24 cell migration and invasion through its negative regulation of c-Met.

MicroRNA-490-5p inhibits proliferation of bladder cancer by targeting c-Fos.

MicroRNAs (miRNAs) are non-protein-coding sequences that play a crucial role in tumorigenesis by negatively regulating gene expression. Here, we found that miR-490-5p is down-regulated in human bladder cancer tissue and cell lines compared to normal adjacent tissue and a non-malignant cell line. To better characterize the function of miR-490-5p in bladder cancer, we over-expressed miR-490-5p in bladder cancer cell lines with chemically synthesized mimics. Enforced expression of miR-490-5p in bladder cancer cells significantly inhibited the cell proliferation via G1-phase arrest. Further studies found the decreased c-Fos expression at both mRNA and protein levels and Luciferase reporter assays demonstrated that c-Fos is a direct target of miR-490-5p in bladder cancer. These findings indicate miR-490-5p to be a novel tumor suppressor of bladder cancer cell proliferation through targeting c-Fos.

MicroRNA-124-3p inhibits cell migration and invasion in bladder cancer cells by targeting ROCK1.

BACKGROUND: Increasing evidence has suggested that dysregulation of certain microRNAs (miRNAs) may contribute to human disease including carcinogenesis and tumor metastasis in human. miR-124-3p is down-regulated in various cancers, and modulates proliferation and aggressiveness of cancer cells. However, the roles of miR-124-3p in human bladder cancer are elusive. Thus, this study was conducted to investigate the biological functions and its molecular mechanisms of miR-124-3p in human bladder cancer cell lines, discussing whether it has a potential to be a therapeutic biomarker of bladder cancer. METHODS: Three human bladder cancer cell lines and samples from ten patients with bladder cancer were analyzed for the expression of miR-124-3p by quantitative RT--PCR. Exogenetic overexpression of miR-124-3p was established by transfecting mimics into T24, UM-UC-3 and J82 cells, after that cell proliferation and cell cycle were assessed by MTT assay, flow cytometry and Colony-forming assay. Cell motility and invasion ability were evaluated by wound healing assay and transwell assay. Tissue microarray, and immunohistochemistry with antibodies against ROCK1, MMP2 and MMP9 was performed using the peroxidase and DAB methods. The target gene of miR-124-3p was determined by luciferase assays, quantitative RT--PCR and western blot. The regulation of epithelial-to-mesenchymal transition by miR-124-3p was analyzed by western blot. RESULTS: miR-124-3p is frequently down-regulated in bladder cancer both in three bladder cancer cell lines, T24, UM-UC-3, J82 and clinical samples. Overexpression of miR-124-3p induced G1-phase arrest in T24, UM-UC-3 and J82 cell lines and suppressed cell growth in colony-forming assay. miR-124-3p significantly repressed the capability of migration and invasion of bladder cancer cells. In addition, ROCK1 was identified as a new target of miR-124-3p. ROCK1, MMP2, MMP9 were up-regulated in bladder cancer tissues. Furthermore, we demonstrated miR-124-3p could inhibit bladder cancer cell epithelial mesenchymal transfer, and regulated the expression of c-Met, MMP2, MMP9. CONCLUSIONS: miR-124-3p can repress the migration and invasion of bladder cancer cells via regulating ROCK1. Our data indicate that miR-124-3p could be a tumor suppressor and may have a potential to be a diagnostics or predictive biomarker in bladder cancer.

Apigenin promotes apoptosis, inhibits invasion and induces cell cycle arrest of T24 human bladder cancer cells.

BACKGROUND: Apigenin (4',5,7-trihydroxyflavone) was recently shown effective in inhibiting several cancers. The aim of this study was to investigate the effect and mechanism of apigenin in the human bladder cancer cell line T24 for the first time. METHODS: T24 cells were treated with varying concentrations and time of apigenin. Cell viability was evaluated by MTT assay. Cell motility and invasiveness were assayed by Matrigel migration and invasion assay. Flow cytometry and western blot analysis were used to detect cell apoptosis, cell cycle and signaling pathway. RESULTS: The results demonstrated that apigenin suppressed proliferation and inhibited the migration and invasion potential of T24 bladder cancer cells in a dose- and time-dependent manner, which was associated with induced G2/M Phase cell cycle arrest and apoptosis. The mechanism of action is like to involve PI3K/Akt pathway and Bcl-2 family proteins. Apigenin increased caspase-3 activity and PARP cleavage, indicating that apigenin induced apoptosis in a caspase-dependent way. CONCLUSIONS: These findings suggest that apigenin may be an effective way for treating human bladder cancer.

Quantitative assessment of the associations between XRCC1 polymorphisms and bladder cancer risk.

BACKGROUND: The XRCC1 polymorphisms have been implicated in bladder cancer risk, but individually published studies show inconsistent results. The aim of our study was to clarify the effects of XRCC1 variants on bladder cancer risk. METHODS: A systematic literature search up to September 13, 2012 was carried out in PubMed, EMBASE and Wanfang databases, and the references of retrieved articles were screened. Crude odds ratios with 95% confidence intervals were used to assess the associations between XRCC1 Arg194Trp and Arg399Gln polymorphisms and bladder cancer risk. Heterogeneity and publication bias were also evaluated. RESULTS: A total of 14 and 18 studies were eligible for meta-analyses of Arg194Trp and Arg399Gln, respectively. Regrouping was adopted in accordance with the most probable appropriate genetic models. No obvious heterogeneity between studies was found. For overall bladder cancer, the pooled odds ratios for Arg194Trp and Arg399Gln were 1.69 (95% confidence interval: 1.25 to 2.28; P = 0.001) and 1.10 (95% confidence interval: 1.03 to 1.19; P = 0.008), respectively. After excluding the studies that were not in Hardy-Weinberg equilibrium, the estimated pooled odds ratio still did not change at all. CONCLUSIONS: The meta-analysis results suggest that XRCC1 Arg194Trp and Arg399Gln polymorphisms may be associated with elevated bladder cancer risk.

Construction of a Co-Expression Network for lncRNAs and mRNAs Related to Urothelial Carcinoma of the Bladder Progression.

Carcinoma of urinary bladder is the most familiar cancer of the urinary tract, with the highest incidence in men. However, its prognosis and treatment have not improved significantly in the last 30 years. The main reason for this may be related to the alteration and regulation of genes. These alterations in genes that play a crucial role in cell cycle regulation may result in high-grade tumors and may alter drug sensitivity. Notably, the role of lncRNA in bladder cancer, especially the lncRNA-mRNA regulatory network, has not been fully elucidated. In this manuscript, we compared RNA sequencing (RNA-seq) data from 19 normal bladder tissues and 411 primary bladder tumor tissues using The Cancer Genome Atlas (TCGA) data bank, subjected differentially expressed mRNAs and lncRNAs to weighted gene co-expression network analysis, and screened out modules highly correlated with tumor progression. Subsequently, a lncRNA-mRNA co-expression network was built, and two key mRNAs were identified via COX regression analysis. Kaplan-Meier curve analysis revealed that the overall survival of sick people in the high-risk section was significantly shorter than those in the low-risk section. Therefore, this lncRNA-mRNA-based co-expression pattern may be used clinically to predict the prognosis of carcinoma of urinary bladder people. Our study not only provides a genetic target for carcinoma of urinary bladder therapy but also provides new ideas for people in the medical profession to discover the treatment of various tumors.

Fluid intake and the risk of bladder cancer: results from the South and East China case-control study on bladder cancer.

Although several studies have assessed the association between total fluid intake, specific drinks and bladder cancer, no firm conclusions can yet be drawn. Four hundred thirty two bladder cancer cases and 392 frequency matched hospital-based controls recruited in the South and East of China between October 2005 and June 2008 were interviewed on their intake of 6 nonalcoholic and 3 alcoholic drinks. Age, sex, smoking and hospital-adjusted odds ratios (OR) and 95 percent confidence intervals (95% CI) were calculated for all drinks and for total fluid intake using logistic regression. For 381 cases (81.9% men) and 371 controls (76.3% men), total fluid intake could be calculated. In men, an increase in total fluid intake was associated with a significantly decreased bladder cancer risk (OR 0.93, 95% CI: 0.88-0.99, per cup fluid consumed). Neither green nor black tea consumption was associated with bladder cancer. Daily consumption of milk significantly reduced the risk of bladder cancer by a half (OR 0.49, 95% CI: 0.32-0.76), which strengthens earlier suggestions that milk is probably associated with a decreased bladder cancer risk. Consumption of wine (OR 0.49, 95% CI: 0.34-0.70) and liquor/spirits (OR 0.65, 95% CI: 0.47-0.92) were associated with a significantly reduced risk. Consumption of water, fruit juice and beer appeared not associated with bladder cancer. There is no clear indication that the risks observed in this Chinese population are substantially different from those observed in Caucasian populations.

The Prognostic Value of Androgen Receptor Splice Variant 7 in Castration-Resistant Prostate Cancer Treated With Novel Hormonal Therapy or Chemotherapy: A Systematic Review and Meta-analysis.

PURPOSE: This study aimed to evaluate the prognostic role of AR-V7 in terms of prostate-specific antigen (PSA) response, progression-free survival (PFS), and overall survival (OS) in CRPC patients treated with novel hormonal therapy (NHT) (Abiraterone and Enzalutamide) or taxane-based chemotherapy (Docetaxel and Cabazitaxel). METHODS: A comprehensive literature search was conducted on PubMed, Embase, and the Web of Science from inception to February 2020. Studies focusing on the prognostic values of AR-V7 in CRPC patients treated with NHT or chemotherapy were included in our meta-analysis. The OS and PFS were analyzed based on Hazard ratios (HRs) and 95% confidence intervals (CIs). Furthermore, Odds ratios (ORs) and 95% CIs were summarized for the AR-V7 conversion after treatment and the PSA response. RESULTS: The AR-V7 positive proportion increased significantly after NHT treatment (OR 2.56, 95% CI 1.51-4.32, P<0.001), however, it declined after chemotherapy (OR 0.51, 95% CI 0.28-0.93, P=0.003). AR-V7-positive patients showed a significantly decreased PSA response rate after NHT (OR 0.13, 95% CI 0.09-0.19, P<0.001) but not statistically significant for chemotherapy (OR 0.63, 95% CI 0.40-1.01, P=0.06). Notably, PFS (HR 3.56, 95% CI 2.53-5.01, P<0.001) and OS (HR 4.47, 95% CI 3.03-6.59, P<0.001) were worse in AR-V7-positive ttreated with NHT. Similarly, AR-V7 positivity correlated with poor prognosis after chemotherapy as evidenced by shorter OS (HR 1.98, 95% CI 1.48-2.66, P<0.001) and a significantly shorter PFS (HR 1.35, 95% CI 0.97-1.87, P=0.07). CONCLUSION: NHT treatment increased AR-V7 positive proportion whereas chemotherapy decreased it. Moreover, AR-V7 positivity correlated with lower PSA response, poorer PFS, and OS in CRPC treated with NHT, and shorter OS in patients receiving chemotherapy.

Correction: Up-regulation of p16 by miR-877-3p inhibits proliferation of bladder cancer.

[This corrects the article DOI: 10.18632/oncotarget.10575.].

Robotic-assisted Urethra-sparing Simple Prostatectomy Via an Extraperitoneal Approach.

OBJECTIVE: To present an original technique of robotic-assisted urethra-sparing simple prostatectomy (RAUSP) for treating patients with benign prostatic hyperplasia. MATERIALS AND METHODS: From April 2015 to December 2016, 27 patients underwent RAUSP via an extraperitoneal approach. Baseline patient characteristics, perioperative outcomes, pathologic outcomes, postoperative Clavien complications, International Prostate Symptom Score, International Index of Erectile Function, and ejaculatory function were assessed. RESULTS: Twenty-six patients (96.3%) successfully underwent RAUSP, one patient (3.7%) was converted to simple prostatectomy. Median operative time was 169 minutes (interquartile range: 150-185); median estimated blood loss was 235 mL (interquartile range: 180-300). Seven cases (26.9%) required urethral repair secondary to inadvertent urethrotomy. Mean catheterization time was 1.6 days (range 1-5). Clavien complications were reported, 6 being low grade (grade 1 or 2) with a single 3a complication (gross hematuria requiring bladder irrigation). Mean follow-up duration was 16.4 months (range 9-30). Postoperative questionnaire demonstrated that international prostate symptom score (P < .001) and quality of life score (P < .001) were significantly improved postoperatively. A total of 14 patients reported erectile function, 13 of which had normal ejaculation, only 1 complained retrograde ejaculation. CONCLUSION: RAUSP is technically feasible for patients with benign prostatic hyperplasia. Our data indicate that patients have short catheterization time, an acceptable risk profile, significant improvements of voiding function and maintaining antegrade ejaculation following this urethral-sparing technique.

Small RNA-induced INTS6 gene up-regulation suppresses castration-resistant prostate cancer cells by regulating ß-catenin signaling.

Small RNAs play an important role in gene regulatory networks. The gene suppressive effect of small RNAs was previously the dominant focus of studies, but during the recent decade, small RNA-induced gene activation has been reported and has become a notable gene manipulation technique. In this study, a putative tumor suppressor, INTS6, was activated by introducing a promoter-targeted small RNA (dsRNA-915) into castration-resistant prostate cancer (CRPC) cells. Unique dynamics associated with the gene upregulation phenomenon was observed. Following gene activation, cell proliferation and motility were suppressed in vitro. Downregulation of Wnt/ß-catenin signaling was observed during the activation period, and the impairment of ß-catenin degradation reversed the tumor suppressor effects of INTS6. These results suggest the potential application of small activating RNAs in targeted gene therapy for CRPC.

Innovative endoscopic enucleations of the prostate - Xie's Prostate Enucleations.

In the past 2 decades, endoscopic enucleation of the prostate has become a safe and effective surgical treatment for benign prostatic hyperplasia (BPH), with comparable outcomes to traditional surgeries. Transurethral vapor enucleation and resection of the prostate (TVERP), transurethral vapor enucleation of the prostate (TVEP), and ultrasound-navigated TVEP (US-TVEP) are new, innovative endoscopic enucleation procedures. These procedures are named Xie's Prostate Enucleations (Xie's Procedures for short). Current clinical data indicate that Xie's Procedures are safe and effective treatment options for patients with BPH, especially for patients with larger prostates. Further prospective, randomized clinical trials compared with traditional transurethral resection of prostate (TURP) are still needed.

Castleman's Disease Presenting in the Pelvis.

Castleman's disease (CD) is a rare benign lymphoid disorder with unknown etiology. There are 2 major forms of this disease, unicentric (ie, localized CD) and multicentric, which play a major role in determining therapy. The mediastinum is the most common localization for the localized CD, whereas its occurrence in the pelvis is even rarer. We report the case of a 22-year-old woman who had a pelvic mass located in the region of the left iliac fossa. The patient subsequently underwent a robotic-assisted laparoscopic tumorectomy. Pathological examination revealed pelvic localized CD of the hyaline-vascular type. CD should be included in the differential diagnosis of pelvic masses that are noted in the pelvic cavity.

MicroRNA-193a-3p inhibits cell proliferation in prostate cancer by targeting cyclin D1.

MicroRNAs (miRNAs) are small non-coding RNAs that affect various biological processes by altering the expression of a target gene. An miRNA microarray analysis has previously revealed a significant decrease in miR-193a-3p levels in prostate cancer tissues compared with that in their benign prostate hyperplasia counterparts. However, the role of miR-193a-3p has yet to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to evaluate the expression levels of miR-193a-3p in two human prostate cancer cell lines. Forced overexpression of miR-193a-3p was established by transfecting mimics into DU-145 and PC3 cell lines. Cell proliferation and the cell cycle were assessed using a cell viability assay, flow cytometry and a colony formation assay. In addition, the target gene of miR-193a-3p was determined by a luciferase assay, RT-qPCR and western blot analysis. The regulation of the cell cycle by miR-193a-3p was also evaluated by western blotting. The results demonstrated that miR-193a-3p expression levels were lower in prostate cancer cell lines as compared with the RWPE normal prostate epithelium cell line. Subsequent gain-of-function studies revealed that stable miR-193a-3p transfection inhibited cell viability, proliferation and colony formation, and induced G1 phase arrest in prostate cancer cells. A luciferase assay and western blot analysis identified cyclin D1 (CCND1) as a direct target gene of miR-193a-3p. In addition, the forced expression of CCND1 was able to counter the inhibitory effects of miR-193a-3p transfection in the prostate cancer cells. In summary, the results suggest that miR-193a-3p may inhibit the viability, proliferation and survival of prostate cancer cells by regulating the expression profile of CCND1, and that miR-193a-3p may be a novel therapeutic biomarker for prostate cancer.