INTRODUCTION:Timosaponin A-III (TAIII) is an effective anti-tumor ingredient extracted from the rhizomes of Anemarrhena asphodeloides. However, the effect of TAIII on prostate cancer cells (PCa) and its underlying mechanisms is rarely investigated. The current study aimed to investigate the anti-tumor effect and potential mechanisms of TAIII in PCa cells. METHODS:The effect of TAIII on the cell proliferation of PCa was evaluated by CCK-8 assay, colony formation assay, and EDU assay. Cell apoptosis and reactive oxygen species (ROS) production were evaluated by flow cytometry. The puncta of LC3 were detected by immunofluorescence analysis. The protein levels of apoptosis, autophagy, and AMPK/mTOR pathway were assessed by western blot. Finally, a PC3 xenograft nude mouse model was constructed to determine the effect of TAIII combined with chloroquine (CQ) in vivo. RESULTS:Our data showed that TAIII inhibited the proliferation of PCa cells and induced ROS-dependent apoptosis. TAIII treatment dramatically promoted the formation of LC3-positive puncta, and increased the expression of LC3B-II and P62 protein. Moreover, the combination of TAIII with CQ significantly enhanced the pro-apoptosis effect of TAIII in PCa cells and the PC3 xenograft model. In addition, the activation of the AMPK/mTOR pathway and the induction of autophagy induced by TAIII were reversed by Compound C. Suppressing AMPK with Compound C enhanced the apoptosis induced by TAIII in PCa cells. DISCUSSION:This study establishes TAIII as a potent anti-prostate-cancer agent that kills tumor cells via ROSdriven apoptosis while simultaneously triggering cytoprotective autophagy through the AMPK-mTOR axis. However, TAIII's clinical potential awaits pharmacokinetic, bioavailability, and toxicity evaluation. CONCLUSION:TAIII induced ROS-mediated cell apoptosis and promoted cytoprotective autophagy via the AMPK/mTOR pathway in PCa. These findings may provide a new strategy for combining TAIII with CQ together for PCa treatment.

Background:Anderson-Hynes pyeloplasty is a classic and highly effective technique for treating congenital ureteropelvic junction obstruction (UPJO). Laparoscopic minimally invasive surgery (MIS) has become the preferred approach for infants and young children. However, a small working area and the complexity of reconstruction procedure pose significant challenges. This study aims to evaluate the efficacy and safety of four-point suspension fixation technique in laparoscopic dismembered pyeloplasty (LDP) for infants and young children with UPJO. Methods:This retrospective cohort enrolled 37 infants and young children diagnosed with UPJO and underwent transperitoneal LDP between 2014 and 2020. The 37 cases were divided into two Groups based on whether suspension fixation was applied during the transperitoneal LDP. Clinical characteristics and follow-up data of these cohorts were retrospectively collected and analyzed. Continuous variables with a normal distribution were expressed as mean ± standard deviation (SD) and analyzed using independent sample t-tests. Non-normally distributed continuous variables were reported as interquartile range (IQR) and analyzed with the Mann-Whitney U-test. Results:In Group A, 21 cases underwent conventional LDP without suspension fixation, while in Group B, 16 cases underwent "suspension fixation" LDP. The operative time (237.9±63.0 vs. 186.4±52.3 min, P=0.01), anastomotic suturing completion time (125.2±21.6 vs. 75.9±12.1 min, P<0.001), and postoperative hospital stay duration [6.0 (4.0, 7.5) vs. 4.5 (3.0, 6.5) days, P=0.04] were significantly shorter in Group B than in Group A, and the intraoperative blood loss [15.0 (5.0, 21.0) vs. 7.5 (5.0, 10.8) mL, P=0.04] in Group B was significantly lower than that in Group A. There were no significant differences between the two Groups in preoperative and anteroposterior renal pelvic diameter (APD), postoperative days to drainage tube removal, and postoperative days to removal of double J (D-J) sent. In Group A, one case developed anastomotic stenosis during follow-up, which improved after ureteral balloon dilation. In Group B, one case developed recurrent febrile urinary tract infection (UTI) within two months of D-J stent removal and was ultimately cured with antibiotic treatment during follow-up. The success rates were 95.2% (20/21) in Group A and 93.8% (15/16) in Group B. Other cases who were followed up showed no recurrence of stenosis, urine leakage, or recurrent UTI. Conclusions:The use of assisted suspension fixation in transperitoneal LDP is safe and efficient for infants and young children, helping to reduce operative time, overcome the small laparoscopic operating area, and address the steep learning curve, making it a valuable approach.

Objective: To describe the surgical technique of robot-assisted single-port laparoscopic redo pyeloplasty (RSLRP) in children and to confirm the feasibility of this technique. Methods: A 12-year-3-month-old boy with recurrent ureteropelvic junction obstruction after robot-assisted laparoscopic surgery underwent RSLRP with da Vinci Xi surgical system. The general clinical characteristics, perioperative variables and follow-up outcomes were summarized. Results: The child was allowed to drink water up to 2 ​h before surgery. The operation was successfully performed without conversion to open surgery or intraoperative complications. The total operative time was 215 ​min, including 170 ​min of console time, with an estimated blood loss of 10 ​mL. Oral intake was initiated postoperatively upon awakening from anesthesia, starting with clear fluids and advancing to a regular diet as tolerated, with no signs of aspiration. The postoperative complication was gross hematuria (Clavien-Dindo grade Ⅱ), which was improved after conservative treatment. The postoperative hospital stay was 7 days, with total hospitalization duration of 11 days. The ureteral stent was removed 35 days after surgery. Follow-up ultrasound showed improvement of hydronephrosis compared with the preoperative assessment. Conclusion: The application of the da Vinci Xi surgical system for pediatric RSLRP is safe and feasible. Further studies with larger cohorts and long-term follow-up are warranted to validate the safety and efficacy of RSLRP in the pediatric population.

BackgroundProstate cancer (PCa) is a prevalent malignancy and a leading cause of cancer-related death among men. Epithelial-mesenchymal transition (EMT) plays a crucial role in tumor progression, metastasis, and treatment. However, there are limited comprehensive studies on the EMT correlation with prognosis, tumor microenvironment, and therapeutic efficacy in PCa.MethodsWe obtained mRNA expression profiles and clinical data of PCa samples, along with 1,011 protein-coding EMT-related genes from public databases. Functional annotation and consensus clustering were performed based on differentially expressed genes. An EMT prognostic signature (EPS) was constructed in the TCGA dataset after a series of bioinformatics analyses and validated in the GSE116918 dataset. The signature was used to explore clinicopathological features, genomic heterogeneity, the immune landscape, and therapy responses. Finally, we examined the expression of key genes in clinical specimens.ResultsAn EPS was established based on four key genes (MEN1, H2AFZ, UCKL1, and FUS). The patients were classified into low-risk and high-risk groups according to their median EPS risk scores. In both datasets, patients in the high-risk group exhibited significantly lower survival rates compared to those in the low-risk group. Furthermore, the EPS risk score proved to be an independent prognostic factor, and the prognostic nomogram based on the EPS risk score and T stage yielded high accuracy. Subsequent investigations found that the EPS risk score was correlated with both tumor mutation burden and genomic heterogeneity. Notably, the low-risk group displayed a higher proportion of tumor-infiltrating immune cells and exhibited better responses to chemotherapy and immunotherapy. As expected, the validation analysis confirmed substantial overexpression of MEN1, H2AFZ, UCKL1, and FUS in PCa tissues relative to adjacent normal prostate tissues.ConclusionOur preliminary EPS represents a promising biomarker for predicting PCa prognosis and has great potential for clinical application.

To evaluate the feasibility and effectiveness of robot-assisted laparoendoscopic single-port surgery (R-LESS) in infant urology and to report our early single-center experience. Clinical data were retrospectively collected from 20 infants (≤ 12 months) who underwent R-LESS using the Da Vinci Xi system between February 2024 and April 2025. Information included demographic characteristics, perioperative parameters, and postoperative outcomes. The median age at surgery was 2.5 (IQR: 2, 4) months. Sixteen patients underwent pyeloplasty, two underwent ureteral reimplantation, and two underwent nephrectomy. All procedures were completed successfully without conversion to open surgery or intraoperative complications. The median docking time, console time, and total operative time were 7 (IQR: 6, 8) min, 181 (IQR: 156, 207) min, and 212 (IQR: 189, 238) min, respectively. Median estimated blood loss was 5 (IQR: 5, 9) mL. Median total hospital stay was 6 (IQR: 6, 10) days, with a median postoperative stay of 2 (IQR: 1, 4) days. The median follow-up duration was 9.1 (IQR: 5.4, 11.2) months. Postoperative complications were observed in three cases (15

No non-invasive biomarkers are clinically available to distinguish aggressive prostate cancer (PCa) from the indolent PCa, as thus may lead the misdiagnose and overtreatment to the patients. This study aims to identify secreted proteins and assess their potentials to discriminate two PCa subtypes. Microarray assay on tissue specimens of the discovery cohort identified secreted genes associated with invasive PCa and macrophage polarization, and the results were validated in an independent cohort. As elevated expression of ΔC499 has been linked to metastatic PCa and poorer prognosis, the relationship of key secretory genes and ΔC499 was investigated. Their roles on macrophage polarization were studied in co-cultured cells, PCa mouse model and patient blood samples. Finally, a multi-gene secreted signature model was developed and tested in training and validation cohorts. ITGB5 was upregulated and TIMP1/TMEM176B were downregulated at RNA level in aggressive Pca, with bioinformatics linking these changes to M2 macrophage polarization. Additionally, we found that ITGB5 expression was positively regulated while TIMP1 and TMEM176B were negatively regulated through distinct transcriptional pathways. Further, we revealed that ΔC499 contributes to ITGB5-driven M2 macrophage polarization, enhancing PCa invasion in vitro and in vivo. Lastly, a multi-gene model integrating ITGB5, TIMP1, and TMEM176B distinguished indolent from aggressive PCa in training cohort (AUC = 0.88) and validation cohort (AUC = 0.90). ΔC499 induces M2 macrophage polarization and drives PCa invasiveness by modulating ITGB5, TIMP1, and TMEM176B. Three genes signature is differentially expressed between aggressive and indolent tumors, providing potential non-invasive biomarkers to discriminate aggressive from indolent PCa.

To compare the therapeutic efficacy of conventional laparoscopic pyeloplasty (LP) and robot-assisted single-port laparoscopic pyeloplasty (RSLP) for ureteropelvic junction obstruction (UPJO) in infants and to summarize the preliminary experience and advantage of RSLP. The clinical data of UPJO infants (≤ 12 months) who received LP and RSLP in our center from October 2018 to October 2024 were analyzed retrospectively. A total of 51 patients with UPJO were included, with 11 cases receiving RSLP (8 with left UPJO; 3 with right UPJO) and 40 receiving LP (29 with left UPJO; 11 with right UPJO). In the RSLP group, the median age was 3 months (range: 1–9 months). In the LP group, the median age was 2.5 months (range: 1–11 months). The mean operative time was 217.45 ± 20.77 min for the RSLP group and 258.57 ± 52.56 min for the LP group. The mean time of ureteropelvic anastomosis in the RSLP group was shorter than that in the LP group (79.36 ± 17.74 vs. 99.35 ± 21.03). The mean hospital stay was 6.27 ± 2.53 days for the RSLP group and 6.32 ± 2.71 days for the LP group. The mean postoperative hospital stay was 1.9 ± 0.94 days for the RSLP group and 2.67 ± 2.37 days for the LP group. The mean hospital costs were 57,950.63 ± 1,165.68 yuan for the RSLP group and 30,396.30 ± 5214.06 yuan for the LP group. Significant improvements in the hydronephrosis grading, anterior–posterior renal pelvic diameters, and renal parenchymal thickness were observed in both groups after surgery. RSLP is a safe and effective method for the treatment of UPJO in infants. Compared with LP, RSLP has the advantages of precise suturing, short anastomosis time, and short operation duration, making it an attractive and safe option. However, it faces the disadvantages of higher cost of hospitalization.

Therapeutic strategies employing mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as promising approaches for renal fibrosis management. Nevertheless, conventional EV production methods suffer from suboptimal yields and functional efficiency, coupled with rapid EV inactivation post-intravenous administration. To address these limitations, we developed a coaxial bioprinting-engineered three-dimensional EVs (3D-EVs) platform integrated with microfluidic fabrication, yielding GM@PACG&3D-EVs hydrogel microspheres with enhanced biocompatibility for targeted renal fibrosis therapy. Comparative analyses revealed the 3D-EVs system's therapeutic superiority over traditional 2D-EVs in both in vitro and in vivo renal fibrosis models (p < 0.05). Through integrated proteomic profiling of EVs and RNA sequencing of tubular epithelial cells (TECs), we identified KLF15 as a critical mediator enriched in 3D-EVs and internalized TECs. This transcription factor orchestrates fatty acid oxidation homeostasis by upregulating FAO-related proteins (CPT1A, ACAA2), suppressing lipid droplet accumulation, mitigating extracellular matrix deposition, and finally alleviating renal fibrosis. The GM@PACG&3D-EVs microspheres demonstrated sustained EV release kinetics over 14 days (cumulative release 44.2 +/- 4.4 %) with enhanced renal retention efficiency (13.1-fold increase vs free EVs), outperforming both GM&3D-EVs and standalone 3D-EV treatments in fibrotic kidney models. This bioengineered 3D-EV manufacturing and delivery paradigm establishes a transformative platform for overcoming current EV therapeutic bottlenecks in renal fibrosis.

Abstract Background Currently, the potential link between aspirin use and the development of prostate cancer remains uncertain. The purpose of this study using two-sample Mendelian randomization (MR) was to elucidate the causal effect of aspirin use on prostate cancer (PCa) risk. Methods This study included pooled statistics from two Genome-Wide Association Study (GWAS), one for aspirin use (61583 cases and 50427 control) and the other for PCa of European descent (22534 cases and 270176 control). Inverse variance weighting (IVW) was used as the main method, MR-Egger method, weighted median method and weighted model method were used to evaluate the causal relationship between aspirin use and PCa risk. Cochran's Q test was used to check the heterogeneity, and the MR-Egger intercept test was used to analyze the horizontal pleotropy of the results, and a residual analysis was carried out to confirm the robustness and reliability of the results. Results Inverse variance weighting was used to infer that aspirin use had a protective effect on reducing the incidence of PCa (OR = 0.986, 95% CI = 0.978–0.994, P = 0.001). Sensitivity analysis showed that pleiotropy and heterogeneity were not observed. Furthermore, the remain-one analysis showed that the survey results were not significantly affected by any instrumental variable. Conclusion There is a causal relationship between aspirin use and the development of PCa, that is, aspirin use reduces the risk of PCa.

Background: Based on publicly available transcriptome and single-cell sequencing data, the current study aimed to explore the molecular mechanisms underlying the involvement of hepatocellular carcinoma-derived growth factor-like 3 (HDGFL3) in prostate cancer (PCA) growth and metastasis. Methods: The Gene Expression Omnibus database was used to download the single cell transcriptome of PCA (GSE193337). Single-cell RNA sequencing (scRNA-seq) data were examined to identify which genes are essential for endothelial cell function. The Cancer Genome Atlas Prostate Adenocarcinoma database provided the RNA sequencing data, and univariate COX regression analysis was introduced to identify the genes that were associated with the prognosis of patients with PCA. Human PCA cell lines PC-3 and DU145 were used in in vitro cellular studies to test the effect of silencing HDGFL3. The results were validated using Transwell® assay, scratch assay, and cell counting kit-8 assay. To support the role of HDGFL3 in PCA, an in vivo animal model of PCA transplantation tumor in nude mice was established. Quantitative reverse transcription polymerase chain reaction was introduced to measure HDGFL3 messenger ribonucleic acid (mRNA) expression levels in tumor tissues from nude mice, and Hematoxylin and Eosin staining was used to identify lung metastasis. Immunohistochemical staining was employed to identify the expression levels of HDGFL3 and hematopoietic progenitor cell antigen CD34+. Results: It was discovered through analysis of the scRNA-seq dataset that HDGFL3, a gene specific to endothelial cells, is linked to a poor prognosis in men with PCA. In addition, HDGFL3 and the expression of genes linked to angiogenesis have a substantial association. Studies on cells in vitro revealed that silencing HDGFL3 prevented PC-3 and DU145 cells from proliferation, migrating and invading. Silencing HDGFL3 decreased the weight of prostate tumors, the number of lung metastases, and the area occupied by CD34+ vascular endothelial cells, according to in vivo investigations. Conclusions: This study identified HDGFL3 as a key gene in endothelial cells that may stimulate tumor angiogenesis to increase the growth and spread of PCA. These results imply that HDGFL3 may represent a possible target for antiangiogenic therapy in the management of PCA.

BackgroundBladder urothelial carcinoma (BLCA) is associated with high mortality and recurrence. Although mRNA-based vaccines are promising treatment strategies for combating multiple solid cancers, their efficacy against BLCA remains unclear. We aimed to identify potential effective antigens of BLCA for the development of mRNA-based vaccines and screen for immune clusters to select appropriate candidates for vaccination.MethodsGene expression microarray data and clinical information were retrieved from The Cancer Genome Atlas and GSE32894, respectively. The mRNA splicing patterns were obtained from the SpliceSeq portal. The cBioPortal for Cancer Genomics was used to visualize genetic alteration profiles. Furthermore, nonsense-mediated mRNA decay (NMD) analysis, correlation analysis, consensus clustering analysis, immune cell infiltration analysis, and weighted co-expression network analysis were conducted.ResultsSix upregulated and mutated tumor antigens related to NMD, and infiltration of APCs were identified in patients with BLCA, including HP1BP3, OSBPL9, SSH3, ZCCHC8, FANCI, and EIF4A2. The patients were subdivided into two immune clusters (IC1 and IC2) with distinct clinical, cellular and molecular features. Patients in IC1 represented immunologically ‘hot’ phenotypes, whereas those in IC2 represented immunologically ‘cold’ phenotypes. Moreover, the survival rate was better in IC2 than in IC1, and the immune landscape of BLCA indicated significant inter-patient heterogeneity. Finally, CALD1, TGFB3, and ANXA6 were identified as key genes of BLCA through WGCNA analysis, and their mRNA expression levels were measured using qRT-PCR.ConclusionHP1BP3, OSBPL9, SSH3, ZCCHC8, FANCI, and EIF4A2 were identified as potential antigens for developing mRNA-based vaccines against BLCA, and patients in IC2 might benefit more from vaccination.

Bladder cancer is one of the most common carcinomas in the human urinary system worldwide. Loperamide, known as an antidiarrheal drug, exerts anti-tumor activities against various cancers. However, the effect of loperamide on bladder cancer cells remains unclear. Our study aimed to investigate the effect of loperamide on bladder cancer and explore the underlying mechanisms. We found that loperamide suppressed the proliferation of 5637 and T24 cells in a dose-dependent manner. Loperamide treatment showed both pro-apoptotic and pro-autophagic effects on bladder cancer cells. Moreover, it was revealed that loperamide induced reactive oxygen species (ROS) accumulation, leading to the activation of c-Jun N-terminal kinase (JNK) signaling pathway. Notably, ROS scavenger N-acetyl-L-cysteine (NAC) and JNK inhibitor SP600125 effectively attenuated the induction of autophagy and apoptosis triggered by loperamide. Finally, blocking autophagy with CQ could significantly enhance the anti-cancer effect of loperamide both in vitro and in vivo. Overall, these findings demonstrated that loperamide induced autophagy and apoptosis through the ROS-mediated JNK pathway in bladder cancer cells. Our results suggest that the strategy of combining loperamide with autophagy inhibitor CQ may provide a therapeutic option for the treatment of bladder cancer.

Kidney renal clear cell carcinoma (KIRC) represents one of the most fatal cancers, usually showing malignant progression and a high tumor recurrence rate. The urokinase-type plasminogen activator receptor (PLAUR) plays a critical role in the initiation and progression of several cancers, including KIRC. However, the function and mechanism of PLAUR in patients with KIRC are still unclear and require further investigation. In the present study, we first explored the expression profile and prognostic values of PLAUR in pan-cancer based on The Cancer Genome Atlas and Genotype-Tissue Expression databases. PLAUR was upregulated in multiple cancers and was significantly associated with poor overall survival and disease-free survival only in patients with KIRC. Subsequently, the PVT1/SNHG15-hsa-miR-532-3p axis was identified as the most potential upstream regulatory network of PLAUR in KIRC. In addition, PLAUR expression was closely associated with tumor-infiltrating immune cells, tumor immunity biomarkers, and immunomodulator expression. Furthermore, we constructed a multiple-gene risk prediction signature according to the PLAUR-related immunomodulators (PRIs). A prognostic nomogram was then developed to predict the 1-, 3-, and 5-year survival probabilities of individuals. In conclusion, our study identified the PVT1/SNHG15-hsa-miR-532-3p-PLAUR axis and a prognostic signature of PRIs, which could be a reference for future clinical research.

Objective:To investigate the expression level of excision repair cross complementary gene 1 (ERCC 1) in PC-3 cells and prostate samples and its relationship with prognosis.Methods:After siRNA ERCC 1 was transfected into PC-3 cells, the expression level of ERCC 1 protein was detected by Western blot. The MTT method detected cell proliferation activity, andthe Transwell test detected cell migration and invasion capabilities. Immunohistochemistry (IHC) was used to detect the expression level of ERCC 1 protein in 80 PCa and 30 BPH samples, and its relationship with pathological characteristics and prognosis was analyzed.Results:After siRNA ERCC 1 plasmid was transfected into PC-3 cells, Western blot showed that the expression level of ERCC 1 was significantly reduced. Transwell test showed that the migration and invasion ability of PC-3 cells after siRNA ERCC 1 expression was significantly decreased (P<0.05). IHC indicated that the positive expression rate of ERCC 1 in PCa samples was 71.3%(57/80), and the high expression rate was 23.8%(19/80; IRS≥6); the positive expression rate in BPH samples was 10% (3/30), all are low expression (IRS<6). The expression of ERCC 1 was significantly correlated with preoperative PSA value, Gleason score, pathological stage (pT), lymph node metastasis and positive margins in PCa patients (P<0.05), but not significantly correlated with age (P>0.05). In PCa patients, the biochemical relapse-free survival (BRFS) with low ERCC 1 expression was significantly longer than that of patients with high ERCC 1 expression (P<0.05). Univariate and multivariate COX regression analysis showed that high ERCC 1 expression and pT were independent risk factors with BRFS.Conclusion:SiRNA ERCC 1 inhibit the proliferation, migration and invasion of PC-3 cells. The positive expression rate of ERCC 1 in PCa samples is higher, which related to poor differentiation and high invasive characteristics. The high expression of ERCC 1 may be one of the independent risk factors for the prognosis of PCa patients.

BACKGROUND:Clear cell renal cell carcinoma (ccRCC) is the most common and lethal renal cell carcinoma (RCC) histological subtype. Ferroptosis is a newly discovered programmed cell death and serves an essential role in tumor occurrence and development. The purpose of this study is to analyze ferroptosis-related gene (FRG) expression profiles and to construct a multi-gene signature for predicting the prognosis of ccRCC patients.METHODS:RNA-sequencing data and clinicopathological data of ccRCC patients were downloaded from The Cancer Genome Atlas (TCGA). Differentially expressed FRGs between ccRCC and normal tissues were identified using 'limma' package in R. GO and KEGG enrichment analyses were conducted to elucidate the biological functions and pathways of differentially expressed FRGs. Consensus clustering was used to investigate the relationship between the expression of FRGs and clinical phenotypes. Univariate and the least absolute shrinkage and selection operator (LASSO) Cox regression analysis were used to screen genes related to prognosis and construct the optimal signature. Then, a nomogram was established to predict individual survival probability by combining clinical features and prognostic signature.RESULTS:A total of 19 differentially expressed FRGs were identified. Consensus clustering identified two clusters of ccRCC patients with distinguished prognostic. Functional analysis revealed that metabolism-related pathways were enriched, especially lipid metabolism. A 7-gene ferroptosis-related prognostic signature was constructed to stratify the TCGA training cohort into high- and low-risk groups where the prognosis was significantly worse in the high-risk group. The signature was identified as an independent prognostic indicator for ccRCC. These findings were validated in the testing cohort, the entire cohort, and the International Cancer Genome Consortium (ICGC) cohort. We further demonstrated that the signature-based risk score was highly associated with the ccRCC progression. Further stratified survival analysis showed that the high-risk group had a significantly lower overall survival (OS) rate than those in the low-risk group. Moreover, we constructed a nomogram that had a strong ability to forecast the OS of the ccRCC patients.CONCLUSIONS:We constructed a ferroptosis-related prognostic signature, which might provide a reliable prognosis assessment tool for the clinician to guide clinical decision-making and outcomes research.

To efficiently remove all recurrent lymph nodes (rLNs) and minimize complications, we developed a combination approach that consisted of 68Gallium prostate-specific membrane antigen (PSMA) ligand positron emission tomography (PET)/computed tomography (CT) and integrated indocyanine green (ICG)-guided salvage lymph node dissection (sLND) for rLNs after radical prostatectomy (RP). Nineteen patients were enrolled to receive such treatment. 68Ga-PSMA ligand PET/CT was used to identify rLNs, and 5 mg of ICG was injected into the space between the rectum and bladder before surgery. Fluorescent laparoscopy was used to perform sLND. While extensive LN dissection was performed at level I, another 5 mg of ICG was injected via the intravenous route to intensify the fluorescent signal, and laparoscopy was introduced to intensively target stained LNs along levels I and II, specifically around suspicious LNs, with 68Ga-PSMA ligand PET/CT. Next, both lateral peritonea were exposed longitudinally to facilitate the removal of fluorescently stained LNs at levels III and IV. In total, pathological analysis confirmed that 42 nodes were rLNs. Among 145 positive LNs stained with ICG, 24 suspicious LNs identified with 68Ga-PSMA ligand PET/CT were included. The sensitivity and specificity of 68Ga-PSMA ligand PET/CT for detecting rLNs were 42.9% and 96.6%, respectively. For ICG, the sensitivity was 92.8% and the specificity was 39.1%. At a median follow-up of 15 (interquartile range [IQR]: 6–31) months, 15 patients experienced complete biochemical remission (BR, prostate-specific antigen [PSA] <0.2 ng ml−1), and 4 patients had a decline in the PSA level, but it remained >0.2 ng ml−1. Therefore, 68Ga-PSMA ligand PET/CT integrating ICG-guided sLND provides efficient sLND with few complications for patients with rLNs after RP.

Genes with cross-cancer aberrations are most likely to be functional genes or potential therapeutic targets. Here, we found a total of 137 genes were ectopically expressed in eight cancer types, of which Holliday junction recognition protein (HJURP) was significantly upregulated in prostate cancer (PCa). Moreover, patients with higher HJURP mRNA and protein levels had poorer outcomes, and the protein levels served as an independent prognosis factor for the overall survival of PCa patients. Functionally, ectopic HJURP expression promoted PCa cells proliferation in vitro and in vivo. Mechanistically, HJURP increased the ubiquitination of cyclin-dependent kinase inhibitor 1 (CDKN1A) via the GSK3β/JNK signaling pathway and decreased its stability. This study investigated the role of HJURP in PCa proliferation and may provide a novel prognostic and therapeutic target for PCa.

Objective:To investigate the safety, efficacy and long-term complications of transurethral domestic 1 470 nm laser vaporization for the treatment of <30 g small-volume benign prostatic hyperplasia.Methods:From October 2017 to September 2018, 45 patients with <30 g small benign prostatic hyperplasia were retrospectively studied, including 20 patients in the TURP group and 25 patients in the 1 470 nm laser group. The general clinical materials, perioperative complications and follow-up data of the two groups were recorded.Results:45 patients were operated successfully, the mean follow-up period was 12.6 months (9-16 months). There were no significant differences in age, prostate volume, IPSS, RUV, Qmax, and QOL baseline data between the two groups (P>0.05). The IPSS, RUV, Qmax and QOL of the two groups were improved compared with those before operation (P<0.05) and there was no significant difference between the two groups (P>0.05). The operation time of the 1 470 nm laser group [(48.6±13.6) min vs (56.8±11.7) min, P=0.038], bladder irrigation duration [(0.8±0.5) d vs (1.5±0.9) d, P=0.001], catheter indwelling time [(2.7±0.6) d vs (4.7±0.9) d, P<0.001] and hospital stay [(4.2±1.2) d vs (5.2±1.9) d, P=0.036] were significantly shorter than those in the TURP group, with less hemoglobin changes before and after surgery [(5.5±2.4) g/L vs (11.6 ±2.7) g/L, P<0.01]. Follow-up period revealed 2 cases of urethral stricture in the TURP group and no urethral stricture in the 1 470 nm laser group.Conclusions:Transurethral domestic 1 470 nm laser vaporization is safe and effective for the treatment of <30 g small-volume benign prostatic hyperplasia, intraoperative bleeding is less and recovery time is shorter when compared with TURP, and no urethral stricture complication was discovered during the follow-up period, which can provide an individualized treatment method for BPH.

Background Recently, basic leucine zipper and the W2 domain-containing protein 1 (BZW1) is reported to be implicated in tumor progression. However, the role of BZW1 in prostate cancer remains unknown. This study is aimed to investigate the expression of BZW1 and its influence on cell proliferation in prostate cancer. Methods The expression levels of BZW1 were measured in 136 cases of prostate cancer and matched adjacent non-cancerous prostate tissues by quantificational real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Then, the effect of BZW1 on cell proliferation was further explored. Results QRT-PCR analysis shown that the mRNA levels of BZW1 in prostate cancer were significantly greater compared with those in matched adjacent non-cancerous prostate tissues (P<0.001). IHC results shown the high-expression rate of BZW1 in prostate cancer and matched adjacent non-cancerous prostate tissues were 68.4% and 32.4%, and the difference was statistically significant (P<0.001). BZW1 high-expression significantly correlated with T stage, lymph node metastasis, prostate specific antigen (PSA) and Gleason score (P<0.05). Patients with BZW1 high-expression presented unfavorable prognosis compared with those with BZW1 low-expression (P=0.002). In addition, CCK-8 and Colony formation assays revealed that BZW1 over-expression significantly promoted cell proliferation in vitro. Tumor xenograft shown BZW1 knockdown significantly inhibited tumor growth in vivo. Moreover, BZW1 overexpression activated the TGF-β1/Smad1/Smad3 pathway. Conclusion BZW1 over-expression predicts poorer prognosis and promotes cell proliferation in prostate cancer by regulating TGF-β1/Smad pathway.

Prostate cancer (PCa) represents one of the most prevalent types of cancers and is a large health burden for men. The pathogenic mechanisms of PCa still need further investigation. The aim of this study was to construct an effective signature to predict the prognosis of PCa patients and identify the biofunctions of signature-related genes. First, we screened differentially expressed genes (DEGs) between PCa and normal control tissues in The Cancer Genome Atlas (TCGA) and GSE46602 datasets, and we performed weighted gene co-expression network analysis (WGCNA) to determine gene modules correlated with tumors. In total, 124 differentially co-expressed genes were retained. Additionally, five genes (ARHGEF38, NETO2, PRSS21, GOLM1, and SAPCD2) were identified to develop the prognostic signature based on TCGA dataset. The five-gene risk score was verified as an independent prognostic indicator through multivariate Cox regression analyses. The expression of the five genes involved in the signature was detected in the Gene Expression Omnibus (GEO), Gene Expression Profiling Interactive Analysis (GEPIA), and Oncomine databases. In addition, we utilized DiseaseMeth 2.0 and MEXPRESS for further analysis and found that abnormal methylation patterns may be a potential mechanism for these five DEGs in PCa. Finally, we observed that these genes, except PRSS21, were highly expressed in tumor samples and PCa cells. Functional experiments revealed that silencing ARHGEF38, NETO2, GOLM1, and SAPCD2 suppressed the proliferation, migration, and invasiveness of PCa cells. In summary, this prognostic signature had significant clinical significance for treatment planning and prognostic evaluation of patients with PCa. Thus, ARHGEF38, NETO2, GOLM1, and SAPCD2 may serve as oncogenes in PCa.