Hypoxia-induced cell proliferation, angiogenesis and EMT may be involved in Benign prostatic hyperplasia (BPH) development. Puerarin is an extract of traditional Chinese medicine and has anti-oxidative stress, anti-inflammation and anti-tumor activities. We proposed to explore the therapeutic effect of Puerarin on BPH development and the possible mechanism of its action. HIF-1 signaling pathway molecules in human BPH samples were assayed. Hypoxia-induced cells model of BPH cells (BPH-1) as well as BPH model in vivo were established and the effect of Puerarin on cell proliferation was measured by EDU staining and CCK8. The level of ROS, SOD was detected using commercially available kits. Formation of HIF-1α/HIF-1β Dimers and HIF-1α-HIF-1β/ AKT1/AP-1 expression was measured and located using immunofluorescence, immunohistochemistry and wester blotting. Results indicated that Puerarin could inhibit cell proliferation, angiogenesis and EMT in hypoxia-induced BPH-1 and prostate of BPH mice. Mechanistically, Puerarin significantly downregulates the HIF-1α-HIF-1β/AKT1/AP-1 signaling axis under hypoxic conditions. These therapeutic effects were substantially attenuated by either the HIF-1α agonist deferoxamine (DFO) or genetic overexpression of HIF-1α/β. Notably, HIF-1β knockdown completely abolished HIF-1α-mediated pathological progression in BPH, including cellular proliferation, angiogenesis, and EMT processes. Our results suggested that hypoxia-induced cell proliferation, angiogenesis and EMT may positively correlate with BPH development and Puerarin might suppress BPH through regulated HIF-1α- HIF-1β/AKT1/ AP-1 especially dimer of HIF-1α and HIF-1β.

Bladder tumor is a common tumor in the urinary system, posing a serious threat to patients’ health and quality of life. The standard surgical method for non-muscle-invasive bladder cancer is the transurethral resection of bladder tumor. As a new type of minimally invasive treatment, transurethral holmium laser has shown unique advantages in the treatment of bladder tumors. This work introduces the epidemiological characteristics of bladder tumors and the limitations of traditional treatment methods and elaborates on the technical principles, development history of holmium laser and its application status in the treatment of bladder tumors. By analyzing clinical research data, it compares therapeutic effects between holmium laser and other treatment methods. It also presents the key points of surgical techniques, perioperative management strategies, and measures for the prevention and treatment of complications. This research discusses the current technical challenges and future development directions in holmium laser treatment, providing references for clinical practice and research.

Repeated intravesical injections of autologous platelet-rich plasma (PRP) have shown promise in alleviating symptoms of non-ulcer interstitial cystitis bladder pain syndrome (IC/BPS), but the underlying mechanisms remain unclear. In this single-center prospective study, 80 patients received four monthly PRP injections, with outcomes assessed by symptom scales, urodynamic parameters, and immune indices in urine and serum. PRP significantly reduced 24-h micturition frequency, numeric rating scale (NRS), O’Leary, pelvic pain and urgency/frequency patient symptom scale (PUF), and self-rating anxiety scale (SAS) scores at post-treatment follow-ups (all p < 0.05), while bladder capacity and voided volume remained unchanged. Serum and urinary inflammatory, iron metabolism, and oxidative stress markers were not significantly altered. PRP improved T-lymphocyte mitochondrial metabolic status, reducing CD4+ and CD8+ T-cell mitochondrial mass and decreasing CD8+ effector memory (Tem) T-cell counts, CD8+ Tem-MMPlow, and CD8+ PD-1+ Tem counts after the fourth injection (all p < 0.05). These immunological parameters positively correlated with symptom severity. Baseline NRS > 4 was associated with worse baseline profiles and selective post-treatment improvements, whereas global response assessment (GRA) stratification showed no significant differences. These findings indicate that repeated intravesical PRP alleviates IC/BPS-related pain and urinary symptoms primarily by reversing T-cell exhaustion and enhancing mitochondrial metabolic status, thus highlighting T-cell immunometabolic modulation as a key therapeutic mechanism.

OBJECTIVE:To investigate the expression of RNA binding protein ELAVL1 in prostate cancer (PCa), especially hormone-sensitive prostate cancer (HSPC), and its relationship with tumor proliferation. This study further aims to reveal the molecular mechanism by which ELAVL1 promotes HSPC proliferation by stabilizing SOX4 mRNA in an m6A-dependent manner. METHODS:The expression of ELAVL1 in PCa tissues and its relationship with prognosis were analyzed in the Cancer Genome Atlas (TCGA) database, and the differences in HSPC and hormone-resistant prostate cancer (HRPC) were compared. And its relationship with prognosis were analyzed in the Cancer Genome Atlas (TCGA) database, and the differences in HSPC and hormone-resistant prostate cancer (HRPC) were compared. Western blot was used to detect ELAVL1 protein expression in PCa cell lines. After ELAVL1 knockdown by siRNA, cell proliferation was evaluated using CCK-8 assays, and changes in downstream target genes were detected by RT-qPCR. Tumor xenograft experiments in nude mice were performed to further assess the impact of ELAVL1 on tumor growth. The interaction between ELAVL1 and SOX4 mRNA was verified by RIP-seq. And the mRNA and protein levels of SOX4 after knockdown of ELAVL1 were detected by RT-qPCR and Western blot, respectively. CCK-8 was used to evaluate the effect of SOX4 knockdown on cell proliferation. MeRIP-qPCR was used to detect the m6A modification level of SOX4 and the effect of knocking down METTL3. RNA pull-down experiments verified the interaction between SOX4 RNA fragments and ELAVL1 protein. RNA stability experiments evaluated the effect of ELAVL1 knockdown on SOX4 mRNA stability. RESULTS:The expression of ELAVL1 in PCa cells was higher than that in normal prostate epithelial cells. The prognosis of patients with high expression of ELAVL1 was significantly worse than that of patients with low expression. In the GSE32269 dataset, the expression level of ELAVL1 in HSPC was significantly higher than that in HRPC. After knocking down of ELAVL1 in LNCaP and VCaP cells, CCK-8 experiments showed that the cell proliferation ability was significantly affected after knocking down ELAVL1, and overexpressed ELAVL1 promoted the proliferation of HSPC cells. The results of in vivo studies showed that knockdown of ELAVL1 significantly inhibited the tumorigenic capacity of LNCaP cells and resulted in a marked reduction in xenograft tumor mass. The levels of SOX4 mRNA and protein in LNCaP and VCaP cells were significantly higher than those in normal prostate epithelial cells RWPE-1. RIP-qPCR confirmed the interaction between ELAVL1 protein and SOX4 mRNA. After knocking down of ELAVL1, the expression levels of SOX4 mRNA and protein were significantly decreased. After knocking down of SOX4, the proliferation ability of LNCaP and VCaP cells was significantly inhibited. CONCLUSION:ELAVL1 is highly expressed in HSPC. High expression of ELAVL1 is associated with the proliferation of HSPC. SOX4 is a downstream molecule of ELAVL1 which promotes the proliferation of HSPC. ELAVL1 enhances the stability of SOX4 mRNA through an m6A-dependent mechanism.

Background and objective:Benign prostatic hyperplasia (BPH) is a major cause of lower urinary tract symptoms (LUTS) in men aged ≥50 yr. Xialiqi capsules are a traditional Chinese medicine mainly used for the treatment of moderate BPH-related LUTS. Methods:We conducted a multicenter, randomized, double-blind, placebo-controlled clinical trial of Xialiqi treatment for 8 wk in a cohort of 395 patients. Changes in BPH-related LUTS were assessed in terms of the International Prostate Symptom Score (IPSS). Irritative and obstructive IPSS subscores and secondary efficacy indicators, including quality of life (QoL) and International Index of Erectile Function (IIEF-5) scores, were also assessed. Safety and tolerability were assessed in terms of adverse events (AEs) and serious AE. Key findings and limitations:At the final time point of 8 wk, the least-squares treatment difference in IPSS between the Xialiqi and placebo groups was -2.33 (95% confidence interval -3.01 to -1.64). Analysis of covariance results suggested that there was no significant difference between the groups in terms of interactions of subgroups or between parameter subgroups. Results for secondary efficacy measures, including Chronic Prostatitis Symptom Index and QoL scores, revealed greater improvement with Xialiqi than with placebo. Safety results show that Xialiqi was well tolerated and AEs were mild. Limitations include the lack of long-term follow-up. Conclusions and clinical implications:Xialiqi was associated with an improvement in LUTS over an 8-wk period among men with moderate BPH symptoms. Patient summary:We looked at the safety and efficacy of Xialiqi capsules for the treatment of benign enlargement of the prostate gland in a large Chinese population. We found that Xialiqi provides an early improvement in urinary symptoms and prostate enlargement in men with moderate symptoms relating to an enlarged prostate.

Metabolic rewiring is a starter for lineage plasticity, which is an important driver of prostate development, tumorigenesis and treatment resistance. Androgen-targeted therapies are central to prostate cancer (PCa) management, yet the mechanisms leading prostate development—particularly the metabolic signaling within basal cells during treatment—remain poorly understood. To fulfill this gap, we used multiple models to reveal the metabolic alterations in prostate basal cells. Our study reveals the role of the RBP4-STRA6 axis in modulating retinol metabolism and transporting retinol from adipocyte into prostate cells, contributing to prostate development and basal cell differentiation during androgen deprivation. Through multi-omics analyses, we demonstrate that RBP4-STRA6 axis dependent retinol metabolism is increased with androgen deprivation. Retinol metabolism rewiring is modulated by the androgen receptor (AR) and can regulate basal cell plasticity under androgen deprivation therapy (ADT). Retinol metabolism maintains prostate basal cell lineage plasticity during hormone therapy through the PPARγ signaling pathway, compensating for the AR signaling pathway inhibition by sustaining energy homeostasis and promoting basal cell differentiation. Notably, we identified a basal cell cluster (BC5) characterized by high Retinol metabolism and activated PPARγ signaling pathway, which plays a crucial role in basal-luminal differentiation and prostate growth. This study underscores the importance of RBP4-STRA6 dependent Retinol metabolism, mediating the crosstalk between adipocytes and prostate basal cells, in maintaining prostate development during hormone therapy and provides a foundation for future clinical interventions and diet strategies aimed at enhancing the sensitivity of androgen deprivation in prostate diseases.

RNA modifications are widely distributed in almost all types of RNA, including mRNA, rRNA, miRNA, circRNA, and lncRNA, which are deeply involved in disease initiation and progression and are emerging therapeutic targets in diseases such as cancer, among which N6-methyladenosine (m6A) is the most abundant mRNA modification. Accumulating studies have demonstrated the critical role of m6A during cancer progression and its therapeutic potential in prostate cancer, which is one of the most common malignancies in men worldwide. Here, we reviewed the emerging roles of m6A regulators, including readers, writers, and erasers, and the downstream m6A-modified mRNA and noncoding RNA in prostate cancer. We also discussed the therapeutic potential of targeting m6A in prostate cancer and summarized the emerging agents and technologies, such as the cutting-edge CRISPR-Cas13 in prostate cancer treatment by targeting m6A regulatory pathways. At last, we elucidated the perspective of developing efficient and specific RNA targeting agents and technological platforms to provide new strategies for treating prostate cancer by targeting RNA modifications.

The pathogenesis of benign prostatic hyperplasia(BPH)is commonly regarded as androgen-dependent.The first FDA-approved androgen-targeted medication for BPH,finaste-ride,achieves its therapeutic effect by selectively inhibit-ing type Ⅱ 5-alpha reductase(SRD5A2).

OBJECTIVE:To evaluate the role of alternating intravesical instillation of Bacillus Calmette-Guérin (BCG) and Pseudomonas aeruginosa (PA) in preventing postoperative recurrence in high-risk non-muscle-invasive bladder cancer (HR-NMIBC). METHODS:We retrospectively reviewed the clinical data from 115 HR-NMIBC cases who underwent transurethral resection of bladder tumors (TURBT) at Gongli Hospital of Shanghai Pudong New Area between March 2021 and January 2023. Patients were grouped based on postoperative management: a control group (n=51) treated with standard gemcitabine instillations and an intervention group (n=64) given alternating BCG and PA instillations. This study assessed 1- and 2-year recurrence, recurrence-free survival, safety (gastrointestinal reactions, fever, bladder irritation symptoms, and hematuria), serum tumor markers, and life quality. Univariate and multivariate Cox proportional hazards analyses were applied to identify the recurrence predictors. A nomogram predictive model was further developed for postoperative recurrence risk estimation, and its performance was later validated. RESULTS:Despite an equivalent 1-year recurrence rate, the intervention group showed a lower 2-year recurrence rate, prolonged recurrence-free survival, and superior safety (fewer adverse events) than controls. The intervention group also showed decreased post-treatment serum tumor marker concentrations and greater life quality enhancement relative to the control cohort. Univariate and multivariate analyses identified tumor number ≥3 (P=0.036), high-grade tumors (P=0.040), and gemcitabine monotherapy (P=0.035) as independent predictors for 2-year recurrence. The nomogram's scoring system reliably associated elevated risk points with heightened recurrence risk, demonstrating strong discrimination and reliable calibration in medium-to-high-risk ranges. CONCLUSIONS:Alternating intravesical BCG and PA instillations markedly decreases 2-year postoperative recurrence on the premise of favorable safety in HR-NMIBC patients.

Androgen deprivation therapies targeting the androgen receptor (AR) signaling pathway are the primary treatment strategy for prostate cancer. However, these therapies often lead to castration resistance. Developing novel agents targeting AR-independent oncogenes is critical to address this challenge, particularly for advanced castration-resistant prostate cancer. This study identified three potential tumor drivers of advanced prostate cancer, including CDC20, DTL, and RRM2, through integrative bioinformatic screening that considered gene dependency using CRISPRi/RNAi database, clinical relevance, and experimental validation with CRISPR-Cas13-mediated gene ablation. Further mechanistic studies revealed that CDC20, DTL, and RRM2 were transcriptionally regulated by the RB1/E2F1 axis, mediating cell cycle progression in prostate cancer. Additionally, we identified novel agents targeting these candidates through virtual screening and drug-sensitive tests, utilizing our established small-molecule library. These agents exhibited superior anti-tumor efficacy compared with AR antagonists in vitro. Our study identified novel prostate cancer therapeutic targets independent of the AR signaling pathway and established a research paradigm for developing anti-tumor agents through integrative cancer bioinformatics and network pharmacology analysis.

Benign prostatic hyperplasia (BPH) affects aging men worldwide. Type 2 diabetes mellitus (T2DM) and BPH are aging related progressive diseases. High glucose (HG) promoted epithelial mesenchymal transformation (EMT) glucose-dependently in BPH cells. Arctigenin has multiple therapeutic functions as anti-tumor and anti-inflammatory. The role of Arctigenin in BPH and mechanism remain to be investigated. We proposed to explore the therapeutic effect of Arctigenin on BPH accompanied with T2DM and the molecular mechanism. EMT-related markers such as E-Cadherin and Vimentin along with Ki67 and MBOAT4/(acylated) Ghrelin/GHS-R in samples from BPH patients with euglycemia or T2DM were measured and the role of Arctigenin in cell proliferation, migration and vascular-like networks formation of BPH and vascular endothelial cells in HG culture and db/db mice (T2DM) with BPH were explored. Our results demonstrated that positive EMT-markers, MBOAT4/(acylated) Ghrelin/GHS-R and cell proliferation were found in HG samples of BPH patients, HG-induced cells and db/db mice. Arctigenin suppresses cell proliferation, cell migration and EMT, angiogenesis formation and attenuates BPH in mice under normal or HG condition. Our study suggested that Arctigenin might alleviate BPH companied with type 2 diabetes mellitus by inhibiting Ghrelin-induced EMT and cell proliferation through regulating MBOAT4/(acylated) Ghrelin/GHS-R.

Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota-particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio-promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed apoptosis via PI3K/AKT/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/AKT/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes-IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary polyphenols in metabolic urological disorders.

Obesity disrupts gut microbiota homeostasis and impairs spermatogenesis; however, microbiota-targeted therapies remain insufficiently explored. In this study, a water-soluble polysaccharide(CSP1) was purified from the medicinal plant Cynomorium songaricum. Structural characterization identified CSP1 as a homogeneous α-glucan (Mw 5776 Da) with a backbone of →4)-α-D-Glcp-(1 → residues and C-6 branching. In high-fat diet (HFD)-induced obese mice, CSP1 administration alleviated testicular dysfunction by enhancing sperm count and motility, restoring serum testosterone levels, and ameliorating histopathological damage and germ cell apoptosis. Mechanistically, CSP1 remodeled the gut microbiota composition by suppressing LPS-producing taxa while enriching beneficial populations including SCFA-producing Lachnospiraceae and Bacteroidota. This reshaping reinforced intestinal barrier integrity, as evidenced by the upregulation of ZO-1, occludin, and MUC2. Consequently, CSP1 treatment led to a favorable shift in gut microbiota-derived metabolites, significantly reducing systemic LPS translocation while increasing beneficial short-chain fatty acids (SCFAs) such as acetate and propionate. These changes collectively inhibited testicular TLR4/MyD88/NF-κB activation and downstream pro-inflammatory cytokines (TNF-α, IL-1β). Fecal microbiota transplantation confirmed the causal role of the gut microbiota in mediating CSP1's protective effects. Our findings establish CSP1 as a gut-microbiota-targeting polysaccharide that alleviates obesity-associated male infertility by orchestrating a beneficial remodeling of the gut microbial ecosystem and its metabolic output, offering a novel therapeutic strategy for metabolic reproductive disorders.

IntroductionProstate cancer (PCa) is one of the most common malignant tumors in men, with increasing incidence and mortality rates, and its treatment still faces many challenges and unmet needs. ELAVL1 (human antigen R, HuR) is an RNA-binding protein that plays a crucial role in the development and progression of various cancers. Studies have shown that ELAVL1 is highly expressed in PCa and that inhibiting its expression significantly reduces prostate cell proliferation and metastasis. However, the clinical application of ELAVL1-targeting therapies remains limited by the lack of effective delivery strategies. In this context, recent advances in nanodelivery systems offer promising solutions, providing both enhanced targeting efficiency and insights for future prostate cancer treatment strategies.ObjectiveThis review aims to explore the potential of ELAVL1-targeted therapy based on nanodelivery systems in PCa, analyze its advantages and challenges, and provide insights into future research directions.MethodsA systematic review of recent literature summarizing the expression characteristics and biological functions of ELAVL1 in PCa was conducted. Additionally, the advantages, challenges, and applications of various nanomaterials in cancer therapy are discussed.ResultsNanodelivery systems have shown significant potential in the treatment of prostate cancer.

Benign prostatic hyperplasia (BPH), characterized by the non-malignant enlargement of the prostate, exhibits a pronounced association with inflammation resulting from androgen receptor (AR) deficiency. Ferroptosis, a cell death mechanism triggered by iron-dependent lipid peroxidation and closely linked to inflammation, has yet to be fully understood in the context of BPH. Using RNA sequencing, we observed a significant elevation of taurine-upregulated gene 1 (TUG1) long noncoding RNA (lncRNA) in BPH tissues compared to normal prostate tissue. High levels of TUG1 exhibited a discernible correlation with both prostate volume and the extent of inflammatory infiltration in BPH patients. The suppression of TUG1 not only led to a reduction in prostate size but also ameliorated AR-deficiency-induced prostatic hyperplasia. Mechanistically, a decrease in AR in prostate luminal cells prompted macrophage aggregation and the release of IL-1β, subsequently fostering the transcription of TUG1 via MYC. Induced TUG1, through competitive binding with miR-188-3p, facilitated the expression of GPX4, thereby diminishing intracellular ROS levels and impeding ferroptosis in prostate luminal cells. Notably, the ferroptosis inducer JKE-1674 alleviated inflammation-induced prostatic hyperplasia in vivo. Together, these findings suggest that AR deficiency crucially inhibits ferroptosis, promoting BPH via the TUG1/miR-188-3p/GPX4 signaling axis, and making ferroptosis induction a promising therapeutic strategy for BPH patients with AR deficiency.

Aims Tumor fatty acid (FA) metabolic plasticity plays a pivotal role in resistance to therapy and poses limitations to anticancer strategies. In this study, our aim is to uncover the role of acetate metabolism in neurodifferentiation (NED)-mediated castration-resistant prostate cancer (CRPC). Methods We conducted analyses using LC-MS/MS on clinical prostate cancer tissue before and after hormone therapy. We established tumor xenograft mouse models, primary tumor cells, and human-derived organoids to detect the novel mechanism of NED and to identify potential therapies. Results The hormone therapy-induced upregulation of acetate metabolism was mediated by acyl-CoA synthetase short-chain family member 2 (ACSS2), which increased c-MYC expression for NED induction. Notably, combined treatment with an ACSS2 inhibitor and enzalutamide significantly reduced the xenograft tumor volume. Conclusion Our findings uncovered the critical role of acetate metabolism in NED-mediated CRPC and suggest that ACSS2 inhibitors may represent a novel, low-toxicity strategy when combined with hormone therapy for treating patients with NED-mediated CRPC.

Objective Proliferative nodular formation represents a characteristic pathological feature of benign prostatic hyperplasia (BPH) and serves as the primary cause for prostate volume enlargement and consequent lower urinary tract symptoms (LUTS). Its specific mechanism is largely unknown, although several cellular processes have been reported to be involved in BPH initiation and development and highlighted the crucial role of epithelial cells in proliferative nodular formation. However, the technological limitations hinder the in vivo investigation of BPH patients.Methods The robust cell type decomposition (RCTD) method was employed to integrate spatial transcriptomics and single cell RNA sequencing profiles, enabling the elucidation of epithelial cell alterations during nodular formation. Immunofluorescent and immunohistochemical staining was performed for verification.Results The alterations of epithelial cells during the formation of nodules in BPH was observed, and a distinct subgroup of basal epithelial (BE) cells, referred to as BE5, was identified to play a crucial role in driving this progression through the hypoxia-induced epithelial-mesenchymal transition (EMT) signaling pathway. BE5 served as both the initiating cell during nodular formation and the transitional cell during the transformation from luminal epithelial (LE) to BE cells. A distinguishing characteristic of the BE5 cell subgroup in patients with BPH was its heightened hypoxia and upregulated expression of FOS. Histological verification results confirmed a significant association between c-Fos expression and key biological processes such as hypoxia and cell proliferation, as well as the close relationship between hypoxia and EMT in BPH tissues. Furthermore, a strong link between c-Fos expression and the progression of BPH was also been validated. Additionally, notable functional differences were observed in glandular and stromal nodules regarding BE5 cells, with BE5 in glandular nodules exhibiting enhanced capacities for EMT and cell proliferation characterized by club-like cell markers.Conclusions This study elucidated the comprehensive landscape of epithelial cells during in vivo nodular formation in patients, thereby offering novel insights into the initiation and progression of BPH.

OBJECTIVE:To investigate the clinical effect of pulsed thulium laser (PTL) combined with triamcinolone acetonide injection in the treatment of failed posterior urethral anastomosis (FPUA). METHODS:This retrospective study included 35 male patients treated in Gongli Hospital for failed posterior urethral anastomosis from January 2018 to December 2023. All the patients underwent direct-vision internal urethrotomy (DVIU) with transurethral PTL (the PTL group, n = 15) or transurethral plasma (the TUP group, n = 20), and all received intralesional injection of triamcinolone acetonide. We followed up the patients for a median of 21 months, recorded the age, length of urethral stricture, operation time, pre- and post-operative maximum urinary flow rate (Qmax), postoperative complications and recurrence of urethral stricture, and compared the data obtained between the two groups. RESULTS:All the patients smoothly completed the treatment procedures. No statistically significant differences were observed in the age, length of urethral stricture, operation time and postoperative complications between the two groups (P > 0.05). The median follow-up time for the thulium laser group and plasma group was 21.0 months (IQR 16.0－24.0) and 21.0 months (IQR 17.0－25.0), respectively, with a statistically significant difference observed in the maximum urine flow rate before and after surgery at the 12-month mark (P < 0.01). No significant disparity was found in terms of relapse-free survival between the two groups (P = 0.398) Conclusion: Pulsed thulium laser combined with triamcinolone acetonide injection can effectively maintain a short-term cicatricial stability of the urethral stricture and satisfactory urethral patency, obviously superior to plasmotomy as a remedial treatment of urethral stricture after failed posterior urethral anastomosis.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the immunohistochemical data shown in Fig. 1C on p. 236, and immunofluorescence data featured in Figs. 2G and 5G on p. 237 and 239 respectively, were strikingly similar to data that had appeared in other articles written by different authors at different research institutes which had already been published.  In view of the fact that certain of the data in the above article had already been published at the time of the paper's submission, the Editor of International Journal of Oncology has decided that this paper should be retracted from the publication. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 56: 232‑242, 2020; DOI: 10.3892/ijo.2019.4922].