Clear cell renal cell carcinoma (ccRCC) is characterized by intratumoral heterogeneity and a complex immune microenvironment, which contribute to disease progression and therapeutic resistance. Although ribosomal proteins have been implicated in tumor biology, the clinical relevance, microenvironmental impact, and biological role of ribosomal protein lateral stalk subunit P0 (RPLP0) in ccRCC remain unclear. We performed a comprehensive investigation integrating bulk transcriptomics (TCGA, GEO, ICGC, ArrayExpress), proteomics (CPTAC, HPA), single-cell RNA sequencing, and spatial transcriptomics to characterize RPLP0 expression, prognostic value, immunological relevance, and spatial distribution in ccRCC. The biological functions of RPLP0 were validated experimentally using clinical tissues (qRT-PCR, immunofluorescence) and ccRCC cell lines. Proliferation, migration, and invasion were assessed via CCK-8, wound healing, and Transwell assays following siRNA-mediated knockdown, with epithelial–mesenchymal transition (EMT) markers evaluated by Western blot. RPLP0 was ubiquitously expressed in normal tissues but significantly upregulated in ccRCC at both the mRNA and protein levels, which was validated in clinical specimens and cell lines. High RPLP0 expression was associated with advanced tumor stage, metastasis, and poor clinical outcomes, and was identified as an independent prognostic factor. Functional enrichment analyses revealed that RPLP0 was closely linked to ribosome-related processes, DNA damage response, cell cycle regulation, and epithelial–mesenchymal transition. Immune analyses demonstrated that elevated RPLP0 expression correlated with M2 macrophages, as well as with enhanced expression of immune checkpoint and antigen presentation–related genes. Single-cell and spatial transcriptomic analyses revealed the preferential enrichment of RPLP0 in the malignant compartment, with spatial transcriptomics further demonstrating a positive correlation with macrophages. Drug sensitivity analyses based on pRRophetic predictions showed that RPLP0-high tumors were associated with higher estimated IC50 values for several targeted therapies, suggesting a potential association between elevated RPLP0 expression and predicted reduced drug sensitivity. Mechanistically, RPLP0 knockdown in vitro significantly inhibited ccRCC cell proliferation, migration, and invasion, and reversed EMT progression by downregulating mesenchymal markers and upregulating the epithelial marker. These findings indicate that RPLP0 is aberrantly upregulated in ccRCC, promoting tumor progression, migration, and invasion by facilitating the EMT process. Furthermore, its close association with immune activation and spatial heterogeneity highlights its potential as a robust prognostic biomarker and a regulator of tumor-microenvironment interactions.

BackgroundBladder urothelial carcinoma (BLCA) is a common urinary malignancy, and the identification of appropriate biomarkers remains a significant challenge. AKAP7 is a molecular scaffolding protein that plays a crucial role in spatially regulating cyclic adenosine monophosphate (cAMP) signaling through its ability to anchor protein kinase A (PKA) to the cytoskeleton. This study aims to explore the expression level, prognostic implications and immune characteristics of AKAP7 in BLCA.MethodsBased on numerous databases, including CCLE, HPA, Harmonizome, TCGA, GEO, GEPIA2, Kaplan-Meier plotters, GENT2, cBioPortal and the COSMIC databases, we explored the expression pattern, prognostic value and gene alteration and mutation of AKAP7. The potential molecular mechanisms of AKAP7 were analyzed via the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Furthermore, using single-cell RNA-seq datasets, we investigated the distribution of AKAP7 in tumor microenvironments (TME). We utilized the TISIDB database to analyze the association between AKAP7 and immune characteristics. Additionally, we explored the correlation between AKAP7 expression and ferroptosis using TCGA and GEO data sets. Finally, we verified the expression level of AKAP7 in clinical samples of BLCA as well as BLCA cell lines.ResultsCompared with normal tissues, we observed a decreased expression level of AKAP7 in BLCA tissues. BLCA patients with low AKAP7 expression showed poor prognosis. The expression of AKAP7 had a significant positive correlation with the infiltration of T helper cells, Tcm, Eosinopoils, TFH, Th17 and CD8 T cells. The TCGA and GEO datasets suggested that the expression of AKAP7 was closely associated with a ferroptosis-related gene Acyl-CoA synthetase long-chain family member 4 (ACSL4).ConclusionAKAP7 may play a critical role in the prognosis and immune regulation of BLCA prognosis. Besides, it is related to ferroptosis. AKAP7 is an effective biomarker in BLCA.

BackgroundVascular dysfunction caused by urethral injury often leads to delayed repair. Exosome from stem cell showed promise in tissue regeneration. But human induced pluripotent stem cell-derived exosomes (hiPSC-Exo) has not been reported the angiogenesis ability in urethral injury repair and their potential mechanisms.MethodThe exosome was extracted from hiPSCs. The in vivo and in vitro experiments were performed to investigate the effects of hiPSC-Exo on angiogenesis. The miRNA-seq bioinformatics, luciferase assay and related functional experiments were performed to determine potential mechanism.ResultExosome was extracted from hiPSCs by ultracentrifugation. Compared to the control group, hiPSC-Exo significantly promoted blood flow supply to the ischemic lower limbs of mice and rat model of urethral defects to accelerate injury repair. We found that hiPSC-Exo significantly enhanced the proliferation, migration, and tube formation ability of endothelial cells in vitro. MiRNA-seq analysis and experiments verified that miR-103a-3p was highly expressed in HUVEC treated with hiPSC-Exo and significantly enhanced the proliferation, migration, invasion, and angiogenesis effects. TGFBR3 was identified as a direct target of miR-103a-3p through bioinformatics, qPCR, and dual luciferase assays. Overexpression of TGFBR3 leaded to reduced proliferative, migrative and angiogenesis ability of HUVEC, but silence could promote HUVEC function. TGFBR3 could decrease VEGF expression and phosphorylation-based activation of FAK.ConclusionThis study indicated that hiPSC-Exo played a crucial role in promoting angiogenesis to accelerate urethral injury repair through the action of miR-103a-3p in exosome on the TGFBR3/VEGF/FAK signaling pathway in endothelial cells. This provides a new treatment strategy for hiPSC-Exo in the clinical treatment of urethral injury healing and elucidates its unique mechanism of action.

In this study, we systematically investigated bladder cancer-related gene signatures using a toxicogenomics-informed framework, with particular attention to genes associated with lactylation-related pathways. Multi-omics data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) were integrated, and Weighted Gene Co-expression Network Analysis (WGCNA), a toxicology database, and lactylation-related gene sets were combined for intersection screening. Machine learning algorithms, including LASSO, SVM, and random forest, were then applied to identify key genes. Four prioritized BPA-lactylation-associated candidate genes-ENO1, WBP11, GTF2F1, and SPR-were ultimately identified and showed consistent associations with metabolic, immune, and transcription-related features. Multi-level validation, including immune infiltration analysis, single-cell transcriptome localization, proteomic validation, and molecular docking and kinetic simulation, supported the structural plausibility of BPA-protein interactions at the molecular level. This study proposes a toxicogenomics-informed, hypothesis-generating framework that prioritizes candidate genes and pathways potentially linking BPA-related signatures with lactylation-associated processes in bladder cancer.

Background:Benign prostatic hyperplasia (BPH) is a common urological condition in aging men, often requiring surgical intervention when medical therapy fails. The 1470-nm diode laser enucleation of the prostate (DiLEP) has emerged as a promising technique, but its efficacy and safety remain to be systematically evaluated. Methods:A systematic literature search was conducted in PubMed, Embase, Web of Science, and Cochrane Library to identify randomized controlled trials (RCTs) investigating 1470-nm DiLEP in the treatment of BPH. Primary outcomes included functional parameters such as International Prostate Symptom Score (IPSS), quality of life (QoL), maximum urinary flow rate (Qmax), and post-void residual urine volume (PVR). Secondary outcomes included intraoperative and perioperative indicators (e.g., operative time, hemoglobin decrease, catheterization duration, bladder irrigation time) and complication rates. Effect sizes were synthesized using appropriate fixed- or random-effects models based on heterogeneity, and reported as mean difference (MD) or odds ratios with 95% confidence intervals. Results:Four RCTs involving 533 patients were included. 1470-nm DiLEP was associated with significantly shorter operative time (MD = -24.43, P < 0.0001), reduced hemoglobin loss (MD = -2.77, P = 0.02), shorter bladder irrigation time (MD = -13.23, P < 0.0001), and reduced catheterization duration (MD = -2.29, P < 0.0001). Functional outcomes such as IPSS, QoL, and Qmax were comparable between groups, but DiLEP showed superior reduction in PVR at 6 and 12 months. No significant differences in complication rates were observed. Conclusion:The 1470-nm DiLEP appears to be a safe and effective surgical option for BPH, with advantages in perioperative outcomes and potential mid-term functional benefits, particularly in improving bladder emptying. Further large-scale, long-term RCTs are needed to confirm these findings.

Collagen galactosyltransferase 1 (COLGALT1), a key enzyme involved in collagen post-translational modification, has been implicated in extracellular matrix remodeling across multiple cancer types, yet its prognostic significance and relationship with the tumor immune microenvironment in clear cell renal cell carcinoma (ccRCC) remain unclear. In this study, we analyzed multi-omics datasets from public repositories to assess COLGALT1 expression patterns, clinical relevance, and prognostic value in ccRCC. Quantitative real-time PCR was performed to validate its expression in renal cancer cell lines and normal renal tubular epithelial cells. Immune infiltration profiles were characterized using multiple computational algorithms, and a competing endogenous RNA network was constructed to explore regulatory mechanisms. Our results demonstrated that COLGALT1 expression was significantly upregulated in ccRCC at both mRNA and protein levels and was positively associated with the infiltration of monocytes, T helper 2 cells, macrophages, regulatory T cells, and natural killer cells. Notably, COLGALT1 expression correlated strongly with markers of M2 macrophages, suggesting a role in promoting an immunosuppressive tumor microenvironment. These findings identify COLGALT1 as a novel prognostic biomarker and potential therapeutic target in ccRCC, highlighting its contribution to extracellular matrix remodeling and immune regulation.

Clear cell renal cell carcinoma (ccRCC) is one of the most common cancers in the urinary system. Studies have shown that circRNAs have potential effects in a variety of human tumors. Studying the important signaling pathways and therapeutic targets of circRNAs is essential to increase understanding of ccRCC. In this present study, we clarified that hsa_circGRHL2 was dramatically decreased in ccRCC tissues and cells, which was closely related to the clinicopathological features of ccRCC patients. Functionally, circGRHL2 significantly inhibited the proliferation, migration, and invasion of ccRCC cells in vitro. Mechanistically, circGRHL2 sponges miR-330-5p, could regulate miR-330-5p to affect proliferation, migration, invasion of ccRCC cells and have effect on epithelial-mesenchymal transition (EMT). Moreover, FBXO21, could be a direct target of miR-330-5p, which further reducing P85 phosphorylation, inhibiting PI3K/AKT pathway activation, and weakening the EMT. In addition, circGRHL2 overexpression enhances the sensitivity of 769-P cells to sunitinib and enhances the ability of sunitinib treatment effects in vivo. In summary, we proposed a novel signaling network, in which circGRHL2 inhibited the progression of ccRCC via the miR-330-5p/FBXO21 axis and decreased PI3K/AKT activation.

BackgroundUpper tract urothelial carcinoma (UTUC) is a relatively rare but aggressive malignancy. Accurate preoperative assessment of tumor grade, invasiveness, and prognosis remains challenging using conventional imaging, cytology, and ureteroscopic biopsy alone. Radiomics and deep learning may provide noninvasive tools for improving risk stratification and clinical decision-making.MethodsThis narrative review summarizes current evidence on radiomics, machine learning, and deep learning in UTUC. Relevant studies were identified from PubMed, Web of Science, and Scopus and synthesized according to clinical applications and methodological considerations.ResultsRadiomics and deep learning models have shown promising performance in pathological grade prediction, differentiation between UTUC and renal cell carcinoma, muscle invasion assessment, and survival or recurrence risk stratification. However, most studies remain retrospective, single-center, and limited by small sample sizes, heterogeneous imaging protocols, inconsistent segmentation methods, insufficient external validation, and limited evidence of clinical utility.ConclusionRadiomics and deep learning are promising approaches for noninvasive preoperative risk stratification in UTUC. Future studies should focus on methodological standardization, multicenter external validation, prospective evaluation, model interpretability, and demonstration of incremental clinical benefit before routine clinical implementation.

Background Bladder and kidney cancer burden rises globally, with environmental toxicants driving their progression. Methods We integrated global epidemiological analysis, single-cell transcriptomics, cell–cell communication analysis, epithelial subclustering, pseudotime inference, toxicological target prediction, survival modeling, cross-cohort validation, single-cell virtual knockout, spatial transcriptomic deconvolution, molecular docking/dynamics, CETSA, and in vitro assays to define a shared molecular interface linking triphenyl phosphate (TPP) to bladder and kidney cancer. Results Both malignancies exhibited age- and SDI-associated burden patterns. Single-cell profiling identified conserved epithelial, stromal, and immune ecosystems, with tumor epithelial cells occupying central positions in intercellular communication networks. Epithelial subclustering revealed a reproducible EMT-high subcluster 4 in both cancers, which localized to a terminal-like pseudotime state and was associated with poor survival. Predicted TPP targets intersected with subcluster 4 signatures and converged on extracellular matrix organization, adhesion, and leukocyte transendothelial migration pathways. Integrative survival modeling and multi-cohort validation identified MMP9 as a robust prognostic candidate associated with tumor progression. Importantly, single-cell virtual knockout of MMP9 revealed convergent remodeling of proliferative, inflammatory, hypoxia-related, and stress-response programs across bladder and renal cancer epithelial cells, highlighting conserved regulatory circuitry. Spatial transcriptomics further localized MMP9 to macrophage- and fibroblast-enriched niches in both tumor types. Structural modeling and CETSA supported an interaction between TPP and MMP9. Experimentally, TPP upregulated MMP9 at both mRNA and protein levels in T24 and 786-O cells; higher concentrations reduced viability, whereas lower concentrations enhanced migration and clonogenic growth. Conclusions TPP promotes the malignant phenotypes of bladder and kidney cancer via MMP9, which is validated by virtual knockout and in vitro experiments.

BackgroundTo evaluate the safety and feasibility of a novel modified laparoscopic radical cystectomy (MLRC) for female bladder cancer patients and to introduce a stepwise description of the modified procedure. MethodsThis retrospective cohort study, conducted from June 2021 to June 2024, included 45 female patients who underwent operative treatment. Perioperative data were compared between the MLRC group (25 patients) and the traditional laparoscopic radical cystectomy (TLRC) group (20 patients). Statistical significance was set at p < 0.05. The MLRC technique was characterized by delayed ureteral clamping to preserve renal function, dissection of the peritoneal reflection was avoided, en bloc resection of the bladder and uterus was performed without dissecting the intervening plane, placing a gauze-packed glove in the vagina for uterine positioning instead of a uterine manipulator, transvaginal specimen extraction, and final pelvic lymph node dissection after specimen removal. ResultsAll operations were completed without conversion to open surgery. The MLRC group had significantly shorter ureteral clamping times (p < 0.001), lower serum potassium concentrations at 2 h postoperation (p < 0.001), less estimated blood loss (p < 0.001), reduced operative time (p < 0.001), shorter pelvic lymph node dissection (PLND) times (p < 0.001), faster time to first postoperative defecation (p < 0.01), fewer complications (p < 0.05) and shorter postoperative hospital stay (p < 0.001). There were no significant differences between the groups in urinary reconstruction, overall survival, local recurrence, distant metastasis, or American Society of Anesthesiologists (ASA) scores. ConclusionMLRC is a safe and feasible approach that offers improved perioperative outcomes compared to traditional laparoscopic procedures.

EPB41L1-5 is known to maintain cell morphology and signal transduction, with evidence suggesting it can inhibit tumor progression. However, its role in kidney renal clear cell carcinoma (KIRC) is not fully understood. This study evaluated EPB41L1-5’s prognostic value in KIRC using bioinformatics methods and validation through qPCR, immunohistochemistry, and cell functional experiments. The results demonstrated a decreased expression of EPB41L in KIRC tissue compared to normal renal tissue, correlating with lower survival rates. Low EPB41L expression was also associated with overall survival in KIRC. Additionally, EPB41L was found to be involved in extracellular matrix regulation, G protein-coupled receptor ligand binding, and multiple immune cell infiltrations. In addition, their elevated methylation levels are associated with poor prognosis in KIRC patients. Overall, EPB41L family is a potential molecular marker for predicting KIRC prognosis, offering insights for therapeutic development.

Clear cell renal cell carcinoma (ccRCC) is an aggressive malignancy with a high risk of postoperative recurrence. Body composition has emerged as a prognostic marker, but its clinical use is hindered by manual measurement methods and poorly interpretable models. This study aimed to develop an automated, interpretable prediction model integrating deep learning-based body composition analysis to assess prognosis and explore underlying mechanisms in advanced ccRCC. This retrospective multicenter study included patients who underwent radical nephrectomy for advanced ccRCC. Body composition was quantified automatically from preoperative CT using a deep learning model (Comp2Comp). These metrics were integrated with clinicopathological features to build machine learning models for predicting 5-year survival and recurrence. Model performance was rigorously evaluated in an independent external cohort. To explore the biological basis of key imaging features, transcriptomic analysis and experimental validation were performed. Metrics for calibration and discrimination were used to compare the models. The multimodal model demonstrated robust predictive performance. The MLP model excelled in 5-year survival prediction (AUC 0.787 internal, 0.812 external), while the SVC model was optimal for recurrence (AUC 0.740 internal, 0.815 external). SHAP analysis identified visceral (VAT) and subcutaneous (SAT) adipose tissue as top predictive features. Subsequent transcriptomic analysis linked VAT to metabolic pathways and SAT to embryonic development programs. Protein expression of key associated genes was confirmed by immunohistochemistry. This study developed an automated multimodal prediction model by integrating deep learning-derived body composition metrics with clinicopathological features, demonstrating promising predictive performance in assessing survival and recurrence risks in advanced ccRCC, which was further supported by a preliminary external validation cohort. SHAP analysis identified visceral and subcutaneous adipose tissue as key predictors. Transcriptomic analysis linked VAT to pathways of mature renal function and SAT to embryonic developmental programs, providing initial insights into potential biological correlates of these imaging biomarkers.

Objective Investigate the function of glutathione reductase-associated protein 5 (GLRX5) and its prognostic significance, as well as its association with CAFs and the TME. Methods Based on data from TCGA and the GEO databases, this study investigates the expression of GLRX5 in BLCA and its association with clinical outcomes. Using the ssGSEA algorithm, we explored the association between functional features of GLRX5 and BLCA. We validated our findings using in vitro cellular functional assays. We explored the regulatory mechanisms associated with GLRX5 using GO, KEGG, and GSEA. Furthermore, based on single-cell and spatial transcriptomics data from bladder cancer, we analyzed the expression patterns and potential functions of GLRX5 in bladder cancer. The results of the above analyses were experimentally explored and validated. Results High expression of GLRX5 in BLCA correlates with malignant biological behavior and poor prognosis. Enrichment analysis indicates that GLRX5 is primarily associated with malignant functional characteristics in bladder cancer, and its expression levels are also linked to EMT, OXPHOS, and FAM. The above analyses have all been validated through in vitro experiments. Single-cell and spatial transcriptomics analyses indicate that GLRX5 is also expressed in CAFs and participates in metabolic pathways. Experiments demonstrated that GLRX5 promotes the activation of CAFs and may enhance tumor cell migration by influencing pathways within the TME. Conclusion High expression of GLRX5 in tumor cells promotes malignant biological behavior and predicts poor prognosis. At the same time, high expression of GLRX5 in CAFs promotes tumor cell migration by affecting the TME.

Background Benign prostatic hyperplasia (BPH) is a common urinary system disease in elderly men, and transurethral resection of the prostate (TURP) is the gold standard for treating BPH. However, this surgery often leads to intraoperative and postoperative bleeding. Tranexamic acid (TXA) is an antifibrinolytic drug commonly used for hemostasis. This study aims to investigate the hemostatic effect of tranexamic acid in TURP surgery. Aim Evaluate the efficacy of tranexamic acid in TURP surgery. Methods We systematically searched the PubMed, Embase, EBSCO, Cochrane Library, and Web of Science databases for randomized controlled trials (RCTs) on TXA treatment for bleeding during transurethral resection of the prostate (TURP), published up to December 2025. Data analysis and management were performed using Review Manager version 5.3. Result After applying the predefined inclusion and exclusion criteria, a total of eight studies involving 611 patients were included in our meta-analysis. The results of our analysis indicated that the TXA group significantly outperformed the control group in three outcomes: intraoperative blood loss (P = 0.04), postoperative 24-hour hemoglobin levels (P < 0.001), and postoperative 24-hour hemoglobin difference (P = 0.02). However, no significant differences were observed between the TXA and control groups regarding surgical time (P = 0.28) and length of hospital stay (P = 0.08). Conclusions Compared to the control group, TXA significantly reduces intraoperative and postoperative bleeding in TURP surgery, making it valuable for anemic patients and in reducing surgical complications.