As one of the most common malignancies of the urinary tract, bladder cancer is the 11th most frequently diagnosed cancer worldwide. 1 Currently, there are approximately 81 190 new cases per year in the United States and 17 240 people die from the disease annually. 2 Although there have been significant advancements in the development of surgical techniques and adjunct treatment, the prognosis of

We combine the telomerase extension reaction and microRNA (miRNA)-induced rolling circle amplification, followed by graphene oxide (GO) and nicking enzyme-assisted signal amplification as a method to analyze telomerase and miRNA-21 in urine samples with the following merits. First, it is a binary assay and can simultaneously output double signals that correspond to the quantities of telomerase and miRNA, respectively. Second, telomerase activity is enhanced by using a DNA molecular beacon probe to inhibit the formation of G-quadruplex. Third, background noise is decreased significantly via introduction of GO. Fourth, performance tests on about 258 urine samples demonstrate that this binary assay can distinguish between urine from bladder cancer patients, those with cystitis, and normal individuals. Finally, this strategy also shows great potential in distinguishing between muscle-invasive bladder cancers and non-muscle-invasive bladder cancers. The proposed strategy will greatly contribute to clinical decision-making and individualized treatments.

BackgroundFew patients with prostate cancer benefit from current immunotherapies. Therefore, we aimed to explore new strategies to change this paradigm.MethodsHuman tissues, cell lines and in vivo experiments were used to determine whether and how N-cadherin impacts the production of programmed death ligand-1 (PD-L1) and indole amine 2,3-dioxygenase (IDO-1) and whether N-cadherin can increase the production of effector (e)Treg cells. Then, we used PC3-bearing humanized non-obese diabetic/severe combined immunodeficiency IL2Rγnull (hNSG) mice with an intravenous injection of human CD34+ hematopoietic stem cells into the tail vein to evaluate whether the N-cadherin antagonist N-Ac-CHAVC-NH2 (designated ADH-1) could improve the therapeutic effect of tumor-infiltrating lymphocyte (TIL)-related treatment.ResultsN-cadherin dramatically upregulated the expression of PD-L1 and IDO-1 through IFN-γ (interferongamma) signaling and increasing the production of free fatty acids that could promote the generation of eTreg cells. In preclinical experiments, immune reconstitution mediated by TILs slowed tumor growth and extended the survival time; however, this effect disappeared after immune system suppression by PD-L1, IDO-1 and eTreg cells. Furthermore, ADH-1 effectively reduced immunosuppression and enhanced TIL-related therapy.ConclusionsThese data show that the N-cadherin antagonist ADH-1 promotes TIL antitumor responses. This important hurdle must be overcome for tumors to respond to immunotherapy.

Abstract. MicroRNAs are small non-coding RNAs, which are critical regulators of carcinogenesis and tumor progression. Previous studies have identified that microRNA-20b (miR-20b) acts as an oncogene in numerous cancers. However, the role of miR-20b in prostate cancer remains unclear. The present study aimed to investigate the expression of miR-20b in prostate cancer and to examine whether modulating miR-20b expression impacts prostate cancer cellular proliferation and migration. It was revealed that miR-20b was strongly expressed in prostate cancer tissues compared with adjacent normal prostate tissues (P<0.05). Knockdown of miR-20b expression by miR-20b inhibitor inhibited VCaP and PC-3 cell growth and migration. Through bioinformatics analysis, phosphatase and tensin homolog (PTEN) was predicted as a target gene of miR-20b in prostate cancer cells, which was validated by dual-luciferase reporter assay and western blot analysis. In addition, restoration of PTEN expression levels did not affect endogenous miR-20b expression in prostate cancer cells. In conclusion, the present study indicated that miR-20b promotes cellular proliferation and migration by directly regulating PTEN in prostate cancer.

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Objectives To describe in detail the techniques for transvesical robot‐assisted radical prostatectomy (RARP) using the da Vinci Si/Xi system (Intuitive Surgical, Sunnyvale, CA, USA) and to evaluate functional and oncological outcomes in 35 patients with prostate cancer. Patients and Methods Thirty‐five patients with localized prostate cancer were enrolled for transvesical RARP. The patients' preoperative data (mean ± sd age 63.4 ± 8.1 years, body mass index 28.6 ± 5.3 kg/m 2 , total prostate‐specific antigen 10.8 ± 4.9 ng/mL and prostate volume 30.6 ± 14.4 mL, and median [interquartile range {IQR}] biopsy Gleason score 6 [6–7], and International Index of Erectile Function [IIEF]‐5 score 18 [16–20]) were collected. Preoperative assessment revealed 28 cases of cT2a and seven cases of cT2b disease. All patients were continent preoperatively (defined as no pad required or one dry pad per day as a precaution). Surgical results and peri‐operative complications were assessed. All patients were followed up for at least 12 months postoperatively. Results The mean operating time was 150 ± 35 min. Estimated blood loss was 100 ± 45 mL. Urinary infection was noted in one patient and managed with levofloxacin. Another patient complained of nocturia on postoperative day 14, which was relieved with solifenacin succinate. Urethral catheters were removed on postoperative day 7. Thirty‐two patients achieved immediate urinary continence, with three patients returning to full continence on postoperative day 14. Postoperative pathology confirmed 24 pT2a cases, nine pT2b cases and two pT2c cases (median [IQR] Gleason score 6 [6–7]). Positive surgical margins were found in four patients (11.4%). No urethral stricture or urinary leakage was noted on urethrocystography taken 3 months after surgery. Urodynamic studies were performed preoperatively and 6 months after surgery: median (IQR) maximum urinary flow 12.2 (10.2–14.9) vs 13.7 (10.1–15.0) mL/s; bladder capacity 385.3 (351.3–410.2) vs 370.2 (330.1–395.4) mL; and voiding phase detrusor contractility 38.5 (27.8–42.3) vs 35.6 (28.3–41.3) mmH 2 O, respectively. During a minimum of 12 months of follow‐up, no biochemical recurrence was noted in any patient. The median (IQR) IIEF‐5 score was 17 (16–19). Conclusions The transvesical approach is a valid alternative to RARP in selected patients, providing promising postoperative urinary continence. Long‐term functional and oncological results require further investigation.

Immune evasion of cancer cells is mainly due to the impaired transduction of apoptotic signals from immune cells to cancer cells, as well as inhibition of subsequent apoptosis signal cascades within the cancer cells. Over the past few decades, the research has focused more on the impaired transduction of the apoptotic signal from immune cells to cancer cells, rather than inhibition of the intracellular signaling pathways. In this study, miR‑221 inhibitor was transfected into bladder cancer cell lines 5637, J82 and T24 to repress the expression of miR‑221. As a result, the repression of miR‑221 on p53 upregulated modulator of apoptosis (PUMA) was abolished, resulting in increased expression of the pro-apoptotic Bax and reduced expression of the anti-apoptotic Bcl-2, which promotes apoptosis of bladder cancer cells. The expression of MMP-2, MMP-9 and VEGF-C were reduced, resulting in reduced invasiveness and infiltration capability of bladder cancer cells, thereby inhibiting the immune evasion of bladder cancer cells.

Background and Objectives: Bladder cancer (BC) is a complex tumor associated with high recurrence and mortality. To discover key molecular changes in BC, we analyzed next-generation sequencing data of BC and surrounding tissue samples from clinical specimens. Methods. Gene expression profiling datasets of bladder cancer were analyzed online. The Database for Annotation, Visualization, and Integrated Discovery (DAVID, https://david.ncifcrf.gov/) was used to perform Gene Ontology (GO) functional and KEGG pathway enrichment analyses. Molecular Complex Detection (MCODE) in Cytoscape software (Cytoscape_v3.6.1) was applied to identify hub genes. Protein expression and survival data were downloaded from OncoLnc (http://www.oncolnc.org/). Gene expression data were obtained from the ONCOMINE website (https://www.oncomine.org/). Results. We identified 4211 differentially expressed genes (DEGs) by analysis of surrounding tissue vs. cancer tissue (SC analysis) and 410 DEGs by analysis of cancer tissue vs. recurrent tissue cluster (CR analysis). GO function analysis revealed enrichment of DEGs in genes related to the cytoplasm and nucleoplasm for both clusters, and KEGG pathway analysis showed enrichment of DEGs in the PI3K-Akt signaling pathway. We defined the 20 genes with the highest degree of connectivity as the hub genes. Cox regression revealed CCNB1, ESPL1, CENPM, BLM, and ASPM were related to overall survival. The expression levels of CCNB1, ESPL1, CENPM, BLM, and ASPM were 4.795-, 5.028-, 8.691-, 2.083-, and 3.725-fold higher in BC than the levels in normal tissues, respectively. Conclusions. The results suggested that the functions of CCNB1, ESPL1, CENPM, BLM, and ASPM may contribute to BC development and the functions of CCNB1, ESPL1, CENPM, and BLM may also contribute to BC recurrence.