Long non‐coding RNAs (lncRNAs) take various biological effects in clear cell renal cell carcinoma (ccRCC) mostly through sponging with microRNAs (miRNAs). lncRNA MIR4435‐2HG is found to promote tumour progression in gastric cancer, glioblastoma and hepatocellular carcinoma. However, the role of lncRNA MIR4435‐2HG in ccRCC progression remains unknown. The purpose of this research was to investigate the potential molecular mechanism of lncRNA MIR4435‐2HG regarding the regulation of ccRCC initiation and progression. In this study, we found the up‐regulation of MIR4435‐2HG in ccRCC tissues and cell lines. Functionally, overexpression of MIR4435‐2HG promoted the proliferation as well as the metastasis in ccRCC cell lines, whereas knockdown of MIR4435‐2HG inhibited the above changes. Then, bioinformatic analysis and luciferase reporter assays confirmed the negative regulation effect of MIR4435‐2HG on miR‐513a‐5p. And further investigations showed that KLF6, which collected from the intersection of databases, was the potential conjugated mRNAs of miR‐513a‐5p. Finally, the rescue experiments revealed the relation among MIR4435‐2HG and KLF6, which showed that KLF6 could reverse the promoting effect of MIR4435‐2HG on ccRCC in vitro and in vivo. Therefore, our findings provided insight into the mechanisms of MIR4435‐2HG in ccRCC and revealed an alternative target for the clinical diagnosis and treatment of ccRCC.

To investigate the potential prognostic role of pre-treatment prognostic nutritional index (PNI) in urinary cancers. Relevant articles were searched comprehensively from PubMed, Embase and Web of Science, up to November 2018. The pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were extracted to evaluate their associations. A total of 12 related articles including 6561 patients were ultimately enrolled. Our results indicated that a relatively lower level of pre-treatment PNI was associated with decreased OS, CSS/DSS and DFS/RFS/PFS (pooled HR = 1.68, 95% CI 1.45–1.95; pooled HR = 1.57, 95% CI 1.33–1.86; pooled HR = 1.75, 95% CI 1.53–1.99, respectively). Subsequent stratified analysis by cancer type for OS showed that PNI could also be a predictor no matter in renal cell cancer (RCC) or bladder cancer (BC) (pooled HR = 1.65, 95% CI 1.37–1.97 and pooled HR = 1.67, 95% CI 1.20–2.33). Similar results could be found in DFS/RFS/PFS (RCC: HR = 1.81, 95% CI 1.54–2.13 and BC: HR = 1.68, 95% CI 1.32–2.12) and in CSS/DSS (RCC: HR = 1.50, 95% CI 1.23–1.82 and upper tract urothelial carcinoma: HR = 1.61, 95% CI 1.13–2.28). As for the treatment subgroup, a relatively lower level of PNI could also be a positive predictor for OS (surgery: HR = 1.64, 95% CI 1.40–1.93; target therapy: HR = 1.88, 95% CI 1.34–2.63) and DFS/RFS/PFS (surgery: HR = 1.69, 95% CI 1.47–1.95; target therapy: HR = 2.14, 95% CI 1.50–3.05). The outcomes of us shed light on that elevated pre-treatment PNI was positively associated with OS, CSS/DSS and DFS/RFS/PFS, indicating that it could be an independent prognostic factor in urinary cancers.

Recent evidences indicated that miRNAs played core role in the progression of clear cell renal cell carcinoma (ccRCC). However, its molecular mechanism in ccRCC is still remained unclear. The study was designed to identify the role and regulatory mechanism of miR-582-5p in ccRCC. In this study, the low expression level of miR-582-5p were detected by qRT-PCR in ccRCC patient tumor samples and ccRCC cell lines, respectively. The expression level of miR-582-5p was associated with tumor stage and metastasis. In vivo and in vitro experiments found miR-582-5p inhibit tumor growth via suppressing COL5A1 expression. Additionally, RUNX1 was identified as the negative regulator of miR-582-5p through database prediction and chromatin immunoprecipitation. Finally, the negative relation of RUNX1 and miR-582-5p was verified through rescue experiment both in vitro and in vivo. In summary, miR-582-5p, which was regulated by RUNX1, inhibited tumor growth and invasion by targeting COL5A1, indicating that miR-582-5p may act as a biomarker and that the RUNX1/miR-582-5p/COL5A1 axis could be a potential therapeutic target for ccRCC.

We evaluated whether glans preserving surgery would be more helpful for patients to regain satisfactory sexual competency postoperatively than conventional partial amputation. From 2004 to 2012 at 4 centers a total of 135 men treated with glans preserving surgery and 36 treated with partial amputation were selected for evaluation from a total of 273 consecutive patients with penile cancer. Subjective evaluation for patient sexual performance was investigated using the IIEF-15. Objective evaluation was done using the audiovisual sexual stimulation test with the RigiScan® Plus. The degree of satisfaction with penile appearance, and patient confidence and partner acceptability for intercourse were evaluated by 5-point scales. Patients treated with glans preserving surgery had better performance in 4 IIEF-15 domains (erectile function, orgasmic function, intercourse satisfaction and overall satisfaction) and 1 RigiScan parameter (tip rigidity) (each p <0.01). They also had significantly higher appearance satisfaction (64.4% vs 13.9%) and intercourse confidence (55.6% vs 5.6%) than men who underwent partial amputation. Sexual partners in the glans preserving group also showed significantly higher appearance satisfaction (51.1% vs 5.6%) and intercourse acceptability (37.8% vs 16.7%) than in the partial amputation group. Glans preserving surgery effectively preserves the functional anatomy and cosmetic appearance of the glans penis. Glans preservation contributes to minimizing postoperative erectile dysfunction and negative psychological impediments, and promotes return to satisfactory sexual performance. Patients treated with glans preservation have more advantages in obtaining sexual acceptance from their partners than those who undergo amputation.

Hypospadias and cryptorchidism are the most common congenital malformations in male neonates, both of which are also the important clinical manifestations of testicular dysgenesis syndrome and share a same origin. Many studies have suggested that prenatal exposure to endocrine-disrupting chemicals (EDCs) is associated with hypospadias and cryptorchidism development. However, the consistent mechanisms remain unclear. To identify the key EDCs, genes and biological networks related to the development of hypospadias and cryptorchidism respectively and commonly, we conduct the present study and found a new method for predicting the correlation between the interactive genes of hypospadias/cryptorchidism and chemicals. Transcriptome profiles were obtained from the Comparative Toxicogenomics Database (CTD). Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analyses and protein-protein interaction (PPI) network were applied for integrative analyses. The rat model and molecular docking were applied to furtherly verifying the findings of the integrative analyses. Besides the highly related genes, most enriched pathways and chemicals for hypospadias and cryptorchidism respectively, we found hypospadias and cryptorchidism share many same highly associated EDCs (e.g., dibutyl phthalate) and genes (e.g., androgen receptor and estrogen receptor 1) through comparing highly related chemicals or genes of hypospadias and cryptorchidism respectively. GO and KEGG analysis showed that these same interactive genes were mainly enriched in steroidogenesis, response to steroid hormone and nuclear receptor activity. PPI network analysis identified 15 biological hub genes. Furtherly, hypospadias and cryptorchidism were induced by prenatal dibutyl phthalate exposure. Decreased serum testosterone level, downregulation of nuclear androgen-dependent and upregulation of cytoplasmic estrogen-dependent pathways may lead to hypospadias and cryptorchidism. This study proposed a new method for predicting the correlation between the interactive genes of hypospadias/cryptorchidism and chemicals and found that hypospadias and cryptorchidism share many same highly associated EDCs and genes.

The advent of high-throughput sequencing methods has facilitated identification of novel long non-coding RNAs (lncRNAs), which have been demonstrated to play an important role in multiple tumors. Moreover, with the assistance of bioinformatics analysis, LINC01605 has been found to be up-regulated in bladder cancer (BC) tissues compared with normal tissues. Hence, the present study was to explore its specific biological role and related mechanism in BC. The relative expression level of LINC01605 was measured in a cohort of BC tissues with matched normal tissues as well as human BC cell lines by quantitative real-time PCR (qRT-PCR). Survival analysis was performed to explore the relationship between LINC01605 expression and the prognosis of BC patients. The biological function of LINC01605 was studied in vitroand in vivo, by means of CCK-8 assay, colony formation assay, transwell assay, and tumor xenografts mice model. LINC01605 was found to be frequently highly expressed in both human BC cells and tissues. Survival analysis indicated that high LINC01605 expression was associated with higher histological grade and clinical stages. In addition, down-regulated LINC01605 in BC cells could significantly inhibit the abilities of proliferation, migration, and invasion in vitro and knockdown of LINC01605 in subcutaneous xenograft tumor model could impede tumorigenesis in vivo. Mechanistically, LINC01605 could activate epithelial–mesenchymal transition (EMT) signaling pathway and promote the expression of matrix metallopeptidase (MMP) 9 (MMP9). In summary, our results shed light on that LINC01605, as a new prognostic biomarker, could promote the proliferation, migration, and invasion of BC cells via activating EMT signaling pathway and up-regulating MMP9 expression.