BACKGROUND PIGU has been proposed as a potential oncogene in bladder cancer (BLCA); however, experimental evidence regarding PIGU expression in BLCA remains lacking, necessitating further investigation into its functions and underlying mechanisms. AIM To explore the expression of PIGU in BLCA and to understand its function and underlying mechanisms. METHODS This study assessed PIGU protein expression in BLCA tissues via immunohistochemistry. We integrated 14 high-throughput datasets from TCGA, GEO, and Array Express to evaluate PIGU's mRNA expression levels and diagnostic efficacy. siRNA-knockdown cell lines were established using the PIGU-overexpressing HT-1376 BLCA cell line. Proliferation capacity was assessed via CCK-8 assays, while apoptosis and cell cycle distribution were evaluated using flow cytometry. PIGU's potential mechanism in BLCA were explored through differential gene enrichment analysis, protein interaction network analysis, and immune infiltration analysis. RESULTS PIGU expression was significantly upregulated in 121 BLCA and 32 non-BLCA samples at the protein level (10.65 +/- 2.14 vs 5.56 +/- 2.68, P < 0.0001) and in 1065 BLCA and 170 non-BLCA samples at the mRNA level (standardized mean difference = 0.74, 95% confidence interval: 0.07-1.41). Elevated PIGU expression correlated with poorer prognosis in BLCA patients, making it an independent prognostic factor. PIGU knockdown inhibited BLCA cell proliferation (P < 0.05), increased apoptosis, and caused cell cycle arrest at the G1 phase. PIGU-regulated genes are enriched in cell cycle pathways, with PCNA and MCM2 serving as hub genes. High PIGU expression was associated with reduced immune cell infiltration and higher tumor purity, potentially promoting immune evasion through VTCN1 activation and ICOS inhibition. CONCLUSION PIGU is upregulated in BLCA and has prognostic value. It promotes tumor progression by regulating the cell cycle and immune microenvironment, showing potential as an effective therapeutic target for BLCA.

Aims This study aimed to characterize cyclin-dependent kinase 1 (CDK1) expression in bladder cancer (BC), elucidate its role in intercellular signaling and mitosis, and identify small-molecule inhibitors targeting CDK1.Methods RNA sequencing data from multiple databases were integrated, with immunohistochemistry on tissue microarrays validating protein expression. Single-cell RNA sequencing (scRNA-seq), spatial transcriptomics (ST), gene set enrichment analysis (GSEA), and molecular docking with molecular dynamics (MD) simulations were performed.Results CDK1 mRNA and protein were significantly overexpressed in BC tissues. CDK1 expression correlated with patient age and race. CDK1 was predominantly expressed in epithelial cells and central to pleiotrophin (PTN) pathway-mediated intercellular communication; virtual CDK1 knockout markedly reduced PTN signaling strength. ST confirmed CDK1 enrichment in tumor regions. GSEA linked CDK1 to mitosis and chromosome segregation, and scRNA-seq analyses revealed a PTN-CDK1-mitosis regulatory axis active specifically in epithelial cells. Dinaciclib showed favorable MD stability as a CDK1 inhibitor.Conclusion CDK1 is significantly overexpressed in BC with good discriminatory ability. Predominantly expressed in BC epithelial cells, CDK1 may be activated by PTN signaling to drive mitosis. MD simulations support Dinaciclib as a promising CDK1-targeting inhibitor.

Mitochondrial dysfunction and damage can result in the release of mitochondrial DNA (mtDNA) into the cytoplasm, which subsequently activates the cGAS-STING pathway, promoting the onset of inflammatory diseases. Various factors, such as oxidative stress, viral infection, and drug toxicity, have been identified as inducers of mitochondrial damage. This study aims to investigate the role of mtDNA as a critical inflammatory mediator in the pathogenesis of ketamine (KET)-induced cystitis (KC) through the cGAS-STING pathway. To investigate the role of the cGAS-STING pathway in KET-induced cystitis, we assessed the expression of cGAS and STING in rats with KET cystitis. Additionally, we evaluated STING expression in conditionally deficient Simian Virus-transformed Human Uroepithelial Cell Line 1 (SV-HUC-1) cells in vitro. Morphological changes in mitochondria were examined using transmission electron microscopy. We measured intracellular reactive oxygen species (ROS) production through flow cytometry and immunofluorescence techniques. Furthermore, alterations in associated inflammatory factors and cytokines were quantified using real-time quantitative PCR with fluorescence detection. We observed up-regulation of cGAS and STING expressions in the bladder tissue of rats in the KET group, stimulation with KET also led to increased cGAS and STING levels in SV-HUC-1 cells. Notably, the knockdown of STING inhibited the nuclear translocation of NF-κB p65 and IRF3, resulting in a decrease in the expression of inflammatory cytokines, including IL-6, IL-8, and CXCL10. Additionally, KET induced damage to the mitochondria of SV-HUC-1 cells, facilitating the release of mtDNA into the cytoplasm. This significant depletion of mtDNA inhibited the activation of cGAS-STING pathway, subsequently affecting the expression of NF-κB p65 and IRF3. Importantly, the reintroduction of mtDNA after STING knockdown partially restored the inflammatory response. Our findings confirmed the activation of the cGAS-STING pathway in KC rats and revealed mitochondrial damage in vitro. These results highlight the involvement of the cGAS-STING pathway in the pathogenesis of KC, suggesting its potential as a therapeutic target for intervention.

BACKGROUND:This study aims to investigate the expression profile, molecular mechanisms, and biological functions of Connective Tissue Growth Factor (CTGF) in bladder cancer (BLCA). METHODS:For accurate CTGF mRNA expression assessment, 1728 samples were collected. Additionally, for uncovering potential signaling pathways, differentially co-expressed CTGF genes were employed. For exploring CTGF's effects, its impact on immune microenvironment and drug sensitivity was studied. RESULTS:CTGF mRNA was significantly underexpressed in BLCA (standardized mean difference [SMD] = -1.06, 95% CI: -1.89-0.23), and this downregulation was confirmed at the protein level (p < 0.0001). CTGF was mainly involved in immune microenvironment-related pathways and biological processes (BPs) associated with stromal remodeling and extracellular matrix dynamics. Moreover, A statistically significant correlation was identified between the expression levels of CTGF and the infiltration degrees of variety of immune cells. Notably, CTGF expression was positively correlated with sensitivity to EGFR inhibitors (e.g., Afatinib) and negatively correlated with resistance to PARP inhibitors (e.g., Olaparib). CONCLUSIONS:This study elucidated the low expression of CTGF in BLCA. CTGF may promotes tumor progression by remodeling the immune microenvironment and extracellular matrix. Additionally, its expression is positively correlated with sensitivity to EGFR inhibitors and negatively correlated with resistance to PARP inhibitors.

BACKGROUND Bladder cancer (BC) is the most common urological tumor. It has a high recurrence rate, displays tutor heterogeneity, and resists chemotherapy. Furthermore, the long-term survival rate of BC patients has remained unchanged for decades, which seriously affects the quality of patient survival. To improve the survival rate and prognosis of BC patients, it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention. Transmembrane 9 superfamily member 1 (TM9SF1), also known as MP70 and HMP70, is a member of a family of nine transmembrane superfamily proteins, which was first identified in 1997. TM9SF1 can be expressed in BC, but its biological function and mechanism in BC are not clear. AIM To investigate the biological function and mechanism of TM9SF1 in BC. METHODS Cells at 60%-80% confluence were transfected with lentiviral vectors for 48-72 h to achieve stable TM9SF1 overexpression or silencing in three BC cell lines (5637, T24, and UM-UC-3). The effect of TM9SF1 on the biological behavior of BC cells was then investigated through CCK8, wound-healing assay, transwell assay, and flow cytometry. RESULTS Overexpression of TM9SF1 increased the in vitro proliferation, migration, and invasion of BC cells by promoting the entry of BC cells into the G2/M phase. Silencing of TM9SF1 inhibited in vitro proliferation, migration, and invasion of BC cells and blocked BC cells in the G1 phase. CONCLUSION TM9SF1 may be an oncogene in BC.

Background:The clinical role of claudin 8 (CLDN8) in kidney renal clear cell carcinoma (KIRC) remains unclarified. Herein, the expression level and potential molecular mechanisms of CLDN8 underlying KIRC were determined. Methods:High-throughput datasets of KIRC were collected from GEO, ArrayExpress, SRA, and TCGA databases to determine the mRNA expression level of the CLDN8. In-house tissue microarrays and immunochemistry were performed to examine CLDN8 protein expression. A summary receiver operating characteristic curve (SROC) and standardized mean difference (SMD) forest plot were generated using Stata v16.0. Single-cell analysis was conducted to further prove the expression level of CLDN8. A clustered regularly interspaced short palindromic repeats knockout screen analysis was executed to assess the growth impact of CLDN8. Functional enrichment analysis was conducted using the Metascape database. Additionally, single-sample gene set enrichment analysis was implied to explore immune cell infiltration in KIRC. Results:A total of 17 mRNA datasets comprising 1,060 KIRC samples and 452 non-cancerous control samples were included in this study. Additionally, 105 KIRC and 16 non-KIRC tissues were analyzed using in-house immunohistochemistry. The combined SMD was -5.25 (95% confidence interval (CI): -6.13 to -4.37), and CLDN8 downregulation yielded an SROC area under the curve (AUC) close to 1.00 (95% CI: 0.99 - 1.00). CLDN8 downregulation was also confirmed at the single-cell level. Knocking out CLDN8 stimulated KIRC cell proliferation. Lower CLDN8 expression was correlated with worse overall survival of KIRC patients (hazard ratio of CLDN8 downregulation = 1.69, 95% CI: 1.2 - 2.4). Functional pathways associated with CLDN8 co-expressed genes were centered on carbon metabolism obstruction, with key hub genes ACADM, ACO2, NDUFS1, PDHB, SDHD, SUCLA2, SUCLG1, and SUCLG2. Conclusions:CLDN8 is downregulated in KIRC and is considered a potential tumor suppressor. CLDN8 deficiency may promote the initiation and progression of KIRC, potentially in conjunction with metabolic dysfunction.

BackgroundThis study aimed to explore the expression level and transcriptional regulation mechanism of Extra Spindle Pole Bodies Like 1 (ESPL1) in bladder cancer (BC).MethodsA multicentre database of samples (n = 1391) was assayed for ESPL1 mRNA expression in BC and validated at the protein level by immunohistochemical (IHC) staining of in-house samples (n = 202). Single-cell sequencing (scRNA-seq) analysis and enrichment analysis explored ESPL1 distribution and their accompanying molecular mechanisms. ATAC-seq, ChIP-seq and Hi-C data from multiple platforms were used to investigate ESPL1 upstream transcription factors (TFs) and potential epigenetic regulatory mechanisms. Immune-related analysis, drug sensitivity and molecular docking of ESPL1 were also calculated. Furthermore, upstream microRNAs and the binding sites of ESPL1 were predicted. The expression level and early screening efficacy of miR-299-5p in blood (n = 6625) and tissues (n = 537) were examined.ResultsESPL1 was significantly overexpressed at the mRNA level (p < 0.05, SMD = 0.75; 95% CI = 0.09, 1.40), and IHC staining of in-house samples verified this finding (p < 0.0001). ESPL1 was predominantly distributed in BC epithelial cells. Coexpressed genes of ESPL1 were enriched in cell cycle–related signalling pathways, and ESPL1 might be involved in the communication between epithelial and residual cells in the Hippo, ErbB, PI3K-Akt and Ras signalling pathways. Three TFs (H2AZ, IRF5 and HIF1A) were detected upstream of ESPL1 and presence of promoter-super enhancer and promoter-typical enhancer loops. ESPL1 expression was correlated with various immune cell infiltration levels. ESPL1 expression might promote BC growth and affect the sensitivity and therapeutic efficacy of paclitaxel and gemcitabine in BC patients. As an upstream regulator of ESPL1, miR-299-5p expression was downregulated in both the blood and tissues, possessing great potential for early screening.ConclusionsESPL1 expression was upregulated in BC and was mainly distributed in epithelial cells. Elevated ESPL1 expression was associated with TFs at the upstream transcription start site (TSS) and distant chromatin loops of regulatory elements. ESPL1 might be an immune-related predictive and diagnostic marker for BC, and the overexpression of ESPL1 played a cancer-promoting role and affected BC patients’ sensitivity to drug therapy. miR-299-5p was downregulated in BC blood and tissues and was also expected to be a novel marker for early screening.

BACKGROUND:Since the start of the 21st century, prostate cancer with lung metastasis (PCLM) has accumulated significant scientific research output. However, a systematic knowledge framework for PCLM is still lacking.AIM:To reconstruct the global knowledge system in the field of PCLM, sort out hot research directions, and provide reference for the clinical and mechanism research of PCLM.METHODS:We retrieved 280 high-quality papers from the Web of Science Core Collection and conducted a bibliometric analysis of keywords, publication volume, and citation frequency. Additionally, we selected differentially expressed genes from global high-throughput datasets and performed enrichment analysis and protein-protein interaction analysis to further summarize and explore the mechanisms of PCLM.RESULTS:PCLM has received extensive attention over the past 22 years, but there is an uneven spatial distribution in PCLM research. In the clinical aspect, the treatment of PCLM is mainly based on chemotherapy and immunotherapy, while diagnosis relies on methods such as prostate-specific membrane antigen positron emission tomography/computed tomography. In the basic research aspect, the focus is on cell adhesion molecules and signal transducer and activator of transcription 3, among others. Traditional treatments, such as chemotherapy, remain the mainstay of PCLM treatment, while novel approaches such as immunotherapy have limited effectiveness in PCLM. This study reveals for the first time that pathways related to coronavirus disease 2019, cytokine-cytokine receptor interaction, and ribosome are closely associated with PCLM.CONCLUSION:Future research should focus on exploring and enhancing mechanisms such as cytokine-cytokine receptor interaction and ribosome and improve existing mechanisms like cadherin binding and cell adhesion molecules.

In search of an effective therapeutic target for bladder urothelial carcinoma (BLCA), the present study aimed to investigate the expression of cyclin B1 (CCNB1) and its putative mechanism in BLCA. BLCA sequencing data from Gene Expression Omnibus and The Cancer Genome Atlas were used to analyze expression of CCNB1 mRNA and high CCNB1 expression had a poorer prognosis compared with those with low expression. Immunohistochemistry (IHC) samples collected from the Human Protein Atlas database were analyzed for CCNB1 protein expression. Short hairpin (sh) CCNB1-transfected BLCA T24 and 5637 cells were used to investigate the effects of CCNB1 and inhibit the proliferation, migration and invasion of BLCA cells, affect the cell cycle distribution and promote apoptosis of 5637 cells. A sh-CCNB1 BLCA chicken embryo chorioallantoic membrane (CAM) transplantation model was established to observe the impacts of sh-CCNB1 on the tumorigenesis of BLCA in vivo. Analysis of sequencing data showed that CCNB1 mRNA was significantly elevated in tumor and BLCA compared with normal tissues [standardized mean difference (SMD)=1.21; 95% CI: 0.26-2.15; I²=95.9%]. IHC indicated that CCNB1 protein was localized in the nucleus and cytoplasm and was significantly increased in BLCA tumor tissues. The in vitro tests demonstrated that proliferation of T24 and 5637 cells transfected with sh-CCNB1 was significantly inhibited and cell migration and invasion ability were significantly decreased. sh-CCNB1 decreased the percentage of T24 cells in G0/G1, 5637 cells in the G0/G1 phase and S phase and increased percentage of 5637 cells in the G2/M phase and increased early apoptosis of 5637 cells. The in vivo experiments demonstrated that the mass of transplanted tumors was significantly decreased compared with the control group following silencing of CCNB1. The present results suggested that CCNB1 was involve in the development and prognosis of BLCA and silencing of CCNB1 may be a promising targeted therapy for BLCA.

Background Previous studies have demonstrated that electrical stimulation of the cerebellar fastigial nucleus (FNS) can considerably decrease infarction volume and improve neurofunction restoration following cerebral ischemia. Nevertheless, the molecular mechanism of the neuroprotective effect of FNS is still vague. Methods In this study, we developed a rat model of ischemia/reperfusion that included 1 h FNS followed by reperfusion for 3, 6, 12, 24, and 72 h. The expression profile of molecular alterations in brain tissues was obtained by transcriptome sequencing at five different time points. The function and pathway of miRNA expression pattern and core genes were annotated by Allen Brain Atlas, STRING database and Cytoscape software, so as to explore the mechanism of FNS-mediated neuroprotection. Results The results indicated that FNS is associated with the neurotransmitter cycle pathway. FNS may regulate the release of monoamine neurotransmitters in synaptic vesicles by targeting the corresponding miRNAs through core Dlg4 gene, stimulate the Alternative polyadenylation (APA) incident’s anti -apoptosis effect on the brain, and stimulate the interaction activation of neurons in cerebellum, cortex/thalamus and other brain regions, regulate neurovascular coupling, and reduce cerebral damage. Conclusion FNS may activate neuronal and neurovascular coupling by regulating the release of neurotransmitters in synaptic vesicles through the methylation of core Dlg4 gene and the corresponding transcription factors and protein kinases, inducing the anti-apoptotic mechanism of APA events. The findings from our investigation offer a new perspective on the way brain tissue responds to FNS-driven neuroprotection.

Objective To establish the normal reference intervals of key risk factors for kidney stones in healthy people in Guangxi, and to provide a basis for intervention measures to prevent stone recurrence. Methods A total of 169 urine samples from 24 hours were collected and analyzed by the Kidney Stones Research Group of the Department of Urology of the First Affiliated Hospital of Guangxi Medical University from May 2022 to October 2022 in Guangxi: 96 cases (37 males, 59 females) volunteers met the enrollment criteria, aged 19 ～ 64 years, and the average age was (41.63±12.68) years. The contents of urine citric acid, oxalic acid, and cystine were detected by liquid chromatography tandem mass spectrometry and compared with reference intervals for other studies. Results There was no significant difference in uric oxalic acid, citric acid, cystine and urine output between men and women (P ＞ 0.05), and compared with foreign reference intervals, uric oxalic acid, citric acid and cystine showed a high proportion of abnormal rates. BMI was inversely correlated with urinary citric acid excretion. Conclusion There are differences between the reference interval established and abroad reference intervals, and it is of some significance to establish the normal reference interval of key metabolic factors related to kidney stones in 24 hours urine at in this region.

Nitidine chloride (NC) is effective on cancer in many tumors, but its effect on bladder cancer (BC) is unknown. We conducted cell function experiments to verify the antineoplastic effect of NC on BC cell lines (5637, T24, and UM-UC-3) in vitro. Then, mRNAs of NC-treated and NC-untreated BC cells were extracted for mRNA sequencing. Differentially expressed genes (DEGs), expression analysis, and drug molecular docking were conducted to discover the target gene of NC. Finally, functional enrichment was analyzed to explore the underlying mechanisms. NC dramatically inhibited proliferation, migration, and invasion, and it induced apoptosis and arrested the S and G2/M phases of BC cell lines. Lymphocyte antigen 75 (LY75) appeared to be the target of NC. LY75 was highly expressed and had the ability to distinguish BC tissue from non-cancerous tissue. Then, drug molecular docking confirmed the targeting relationship between NC and LY75. Gene enrichment analysis showed that the downregulated genes, after being treated with NC, were mainly enriched in pathways relevant to cell pathophysiological processes. NC inhibits BC cell proliferation, migration, and invasion, induces apoptosis, and arrests cell cycles by downregulating the expression of LY75. This study provides molecular and theoretical bases for NC treatment of BC.

Abstract The progression of prostate cancer (PCa) leads to poor prognosis. However, the molecular mechanism of PCa is still not completely clear. This study aimed to elucidate the important role of centromere protein A (CENPA) in PCa. Large numbers of bulk RNA sequencing (RNA‐seq) data and in‐house immunohistochemistry data were used in analysing the expression level of CENPA in PCa and metastatic PCa (MPCa). Single‐cell RNA‐seq data was used to explore the expression status of CENPA in different prostate subpopulations. Enrichment analysis was employed to detect the function of CENPA in PCa. Clinicopathological parameters analysis was utilised in analysing the clinical value of CENPA. The results showed that CENPA was upregulated in PCa (standardised mean difference [SMD] = 0.83, p = 0.001) and MPCa (SMD = 0.61, p = 0.029). CENPA was overexpressed in prostate cancer stem cells (CSCs) with androgen receptor (AR) negative compared to epithelial cells with AR positive. CENPA may influence the development of PCa through affecting cell cycle. Patients with nodal metastasis had higher expression level of CENPA. And patients with high CENPA expression had poor disease‐free survival. Taken together, Overexpression of CENPA may influence the development of PCa by regulating cell cycle and promoting metastasis.

目的 联合基因芯片或RNA测序技术及免疫组织化学染色探究CLDN8在乳头状肾细胞癌(PRCC)中的表达及其临床意义.方法 通过Gene Expression Omnibus数据库、Sequence Read Archive数据库、Array Express数据库、癌症基因组图谱(TCGA)数据库收集PRCC的组织mRNA表达数据集和开展免疫组织化学染色实验检测CLDN8的表达水平,非配对独立样本t检验用于分析CLDN8在癌组织与非癌组织的表达差异.数据偏倚通过Deeks'和Egger's检验评价.标准化均数差(SMD)、灵敏度、特异度、似然比、汇总受试者工作特性曲线用于评估CLDN8的临床价值.收集TCGA数据库中PRCC患者的临床病理参数,通过非配对独立样本t检验或方差分析探究CLDN8表达与患者临床病理特征之间的关系.结果 共筛选出7个数据集,包括500例PRCC组织和111例非癌组织,CLDN8在PRCC中显著低表达(SMD=-6.80,95％CI:-8.97～-4.63),在PRCC与非癌组织表达差异具有极显著统计学意义(P＜0.000 1),汇总受试者工作特性曲线下面积趋近于 1.00(95％CI:0.99～1.00),灵敏度为 0.99(95％CI:0.93～1.00),特异度为 0.99(95％CI:0.83～1.00),阳性、阴性似然比分别为103.39(95％CI:5.16～2 069.90)、0.01(95％CI:0.00～0.08).整体未检测到明显的发表偏倚.CLDN8表达水平与患者性别、年龄、分级分期无明显关联.结论 CLDN8表达水平在PRCC中降低,可能与PRCC的发生、发展相关.

miR-212-5p has been reported to be involved in many biological processes. However, the role of miR-212-5p in ischemic stroke remains unclear. This study explored the biological role and potential mechanism of miR-212-5p in ischemic stroke by investigating the lncfos/miR-212-5p/CASP7 axis. A total of 32 patients with ischemic stroke and 32 age- and sex-matched healthy controls (HCs) were enrolled in this study. In addition, 336 rats were used in this study. The rats were subjected to middle cerebral artery occlusion (MCAO) and intracerebroventricular injection of a microRNA (miRNA) agomir, a miRNA antagomir, a short hairpin RNA (shRNA) lentiviral vector, or a negative control. The neurological deficit score was calculated; the infarct volume was measured; histopathological assays were performed; the neuronal apoptosis rate was determined; and the lncfos, miR-212-5p, and CASP7 expression levels in the peri-infarct area were assessed. In this study, we found that the expression level of miR-212-5p was significantly downregulated in the peri-infarct area and blood of the MCAO model rats and the blood of patients with ischemic stroke. A double-luciferase experiment showed that CASP7 was a direct target gene of miR-212-5p and that miR-212-5p was a target miRNA of lncfos. Lateral ventricular injection of the miR-212-5p agomir effectively inhibited the apoptosis induced by ischemic brain damage, reduced the infarct volume, attenuated the neurological deficit symptoms, and downregulated the expression of CASP7 in the peri-infarct area of the MCAO model rats. Suppressing lncfos with sh-fos led to the upregulated expression of miR-212-5p and played a neuroprotective role in the rat MCAO models. We concluded that miR-212-5p plays a neuroprotective role in ischemic stroke and that its function is regulated by the lncfos/miR-212-5p/CASP7 axis. Moreover, miR-212-5p may be a potential biomarker and therapeutic target for ischemic stroke.

Abstract Bladder cancer (BC) is a common cancer worldwide with a high prevalence. This study was conducted to elucidate the expression and clinical significance of Sorbin and SH3 domain‐containing protein 1 (SORBS1) in BC as well as to explore its molecular mechanism in BC tumourigenesis. RNA‐sequencing data, microarray, and Immunohistochemistry (IHC) were applied to elucidated the SORBS1 expression at multiple levels. After that, the relationship between tumour‐immune infiltration and SORBS1 was also explored. Finally, SORBS1‐related genes in BC were identified to perform functional enrichment analyses. The expression integration revealed that the comprehensive expression of SORBS1 at the mRNA level was −1.02 and that at the protein level was −3.73, based on 12 platforms, including 1221 BC and 187 non‐BC samples. SORBS1 was negatively correlated with tumour purity (correlation = −0.342, p < 0.001) and positively correlated with macrophage (correlation = 0.358, p < 0.001). The results of enrichment analyses revealed that the most significant biological pathways of SORBS1‐related genes were epithelial‐mesenchymal transition. SORBS1 was significantly down‐regulated in BC and may play a role as tumour suppressor. This study provides new directions and biomarkers for future BC diagnosis.

Objective:To investigate the feasibility and safety of suprapubic bladder puncture and gland fixation in transurethral enucleation of the prostate.Methods:The clinical data of 15 patients with benign prostatic hyperplasia admitted to the First Affiliated Hospital of Guangxi Medical University from January 2020 to June 2020 were retrospectively analyzed. The age was (70.27±5.35) years old, preoperative serum prostate-specific antigen (PSA) level was (3.03±1.37) ng/ml, preoperative total prostate weight was 80.3(70.49, 96.78)g, preoperative postvoid residual urine volume(PVR)was 80 (55, 108)ml, and the maximum urine flow rate (Q max) was (6.13±2.25) ml/s. The international prostate symptom score(IPSS) was 25(22, 27), quality of life (QOL)score was 5(5, 6), international erectile function index-5 (IIEF-5) score was (15.38±5.10). All 15 patients underwent conventional transurethral plasma enucleation of prostate by using the three-lobe method, and the enucleated gland was pushed into the bladder completely. Then a laparoscopic pneumoperitoneum needle was used to perform suprappubic cystipuncture, and ureteral grasping forceps were inserted through the outer sheath. The forceps were used to fix the enencied gland. A rapid harvesting electric resection was performed in the broad space of the bladder, and the Ellick was rinsed to remove the tissue fragments. Surgical indicators and complications were recorded. The improvement of subjective score (IPSS, QOL, IIEF-5) and objective index (Q max, PVR) was compared between preoperative and postoperative. Results:All the 15 operations were completed successfully and there were no complications such as blood transfusion, capsule perforation, transurethral resection syndrome, bladder injury, bladder puncture site laceration and bleeding. The weight of resected prostate tissue was 44(40, 60)g, with blood loss (79.20±18.93)ml.The time of enucleation operation was (54.13±10.88)min, with harvest cutting time (14.67±2.50)min, evisceration efficiency (0.89±0.08)g/min, harvesting efficiency (3.26±0.36)g/min, bladder irrigation time (2.47±0.52) d. The time of indwelling catheter was (3.73±0.80)d.The postoperative hospital stay was (4.40±0.91) d. Temporary urinary incontinence occurred in 1 case after operation. All patients were followed up for 6 months after operation. The IPSS score was 3(2, 3), QOL score was 0(0, 1), IIEF-5 score was (20.12±2.30), Q maxwas (21.80±2.14) ml/s and PVR was 10(5, 15)ml, which were all significantly different compared with those before surgery ( P<0.05). The symptoms of the patients were significantly improved. Conclusions:Transurethral plasma enucleation of prostate combined with suprapubic bladder puncture and fixed gland is effective in the treatment of benign prostatic hyperplasia. The subjective symptoms and objective examination of patients have been significantly improved, and no adverse operation-related complications have occurred. It is a suitable method for enucleation of prostate in units which are not equipped with transurethral tissue planer.

Background: Leucine zipper protein 2 (LUZP2) is a vital gene encoding leucine zipper protein. It is of great importance in the incidence and progress of several human cancers. However, little is known about the role and clinical effects of LUZP2 in prostate cancer (PCa). Therefore, it is crucial to unravel the clinicopathological value of LUZP2 in PCa. In all, 1467 PCa and 549 non-prostate cancer (non-PCa) prostate samples were collected from mRNA chip and RNA-sequencing datasets. The protein levels of LUZP2 were verified in 91 prostate gland tissues by in-house immunohistochemistry (IHC). The standardized mean difference (SMD) was calculated to analyze LUZP2 expression. Survival analysis was also conducted to explore the prognostic significance of LUZP2 in PCa. R software was employed to identify the upregulated differently expressed genes (up-DEGs) and coexpressed genes (CEGs) of LUZP2. Additionally, we explored the prospective molecular mechanism of CEGs of LUZP2 through GO and KEGG pathway analyses. Results: Compared with non-PCa, LUZP2 showed predominantly higher expression in PCa (SMD = 1.05, AUC = 0.88). IHC indicated the protein expression level of LUZP2 was consistently upregulated in PCa tissues (SMD = 2.23, 95%CI: 1.67-2.79). LUZP2 upregulation had an AUC of 0.88 (95%CI: 0.85-0.90) to distinguish PCa from non-PCa tissues. KEGG pathway analysis showed that the pathways of amino sugar and nucleoside sugar metabolism were chiefly enriched with the LUZP2 CEGs in PCa. Conclusion: LUZP2 upregulation might play a promoting function in the occurrence of PCa. How to cite: Li S-H, Yang Y-P, He R-Q, et al. Comprehensive expression analysis reveals upregulated LUZP2 in prostate cancer tissues. Electron J Biotechnol 2022;59. https://doi.org/10.1016/j.ejbt.2022.06. 001 (c) 2022 Pontificia Universidad Catolica de Valparaiso. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

目的 探究CLDN8在肾嫌色细胞癌(chRCC)中的表达及临床意义.方法 通过Gene Ex-pression Omnibus、Sequence Read Archive、ArrayExpress及癌症基因组图谱(TCGA)、Genotype-Tissue Ex-pression(GTEx)数据库获取相关数据集,分析chRCC组织、非chRCC组织CLDN8 mRNA表达水平,同时使用自购的组织芯片(In-house TMA数据集)分析chRCC组织、非chRCC组织CLDN8蛋白表达水平,绘制汇总受试者工作特征(sROC)曲线,分析CLDN8诊断效能.结果 共纳入5个数据集.在TCGA-GTEx数据集中,chRCC组织CLDN8 mRNA表达水平高于非chRCC组织,差异有统计学意义(P<0.05).在In-house TMA数据集中,chRCC组织CLDN8蛋白表达水平与非chRCC组织比较,差异有统计学意义(P<0.0001).5个数据集合并标准化均数差为1.33(95％CI:0.39～2.27).CLDN8诊断chRCC的sROC曲线下面积、灵敏度、特异度、阳性似然比及阴性似然比分别为0.93、0.86、0.87、6.78、0.17.结论 CLDN8高表达可能与chRCC形成与进展相关.