Background: Bladder cancer is a leading cause of cancer-related deaths all over the world. Epidemiological studies of bladder cancer are therefore crucial for policy making. This study was carried out to describe the characteristics of changes in the incidence and mortality of bladder cancer from 1990 to 2016 by age group, gender, geographical region, and sociodemographic index (SDI) and to simultaneously project future trends up to 2030.Methods: Incidence and mortality trends in bladder cancer from 1990 to 2016 were described based on data and methodologies from the Global Burden of Disease (GBD) Study. The data also allowed the future trends of bladder cancer incidence and mortality to be predicted by ARIMA model. Trends were analyzed by age group, gender, and SDI. Projections to 2030 were sub-analyzed by SDI countries. R software (x64 version 3.5.1), SAS (version 9.3), and SPSS (version 22.0) were used throughout the process.

Background: This study aims to explore and project the temporal trends in incidence and mortality of testicular cancer. Moreover, it can provide theoretical guidance for the rational allocation of health resources.Methods: This study analyzed existing data on testicular cancer morbidity and mortality from 1990 to 2016 and predicted time-varying trends of age-standardized incidence rate (ASIR) and age-standardized death rate (ASDR) from 2017 to 2030 in different ages, regions and sociodemographic index (SDI) quintile sub-groups.

PurposeTo assess the diverse cell populations of human corpus cavernosum in patients with severe erectile dysfunction (ED) at the single-cell level.MethodsPenile tissues collected from three patients were subjected to single-cell RNA sequencing using the BD Rhapsody™ platform. Common bioinformatics tools were used to analyze cellular heterogeneity and gene expression profiles from generated raw data, including the packages Seurat, Monocle, and CellPhoneDB.ResultsDisease-related heterogeneity of cell types was determined in the cavernous tissue such as endothelial cells (ECs), smooth muscle cells, fibroblasts, and immune cells. Reclustering analysis of ECs identified an arteriole ECs subcluster and another one with gene signatures of fibroblasts. The proportion of fibroblasts was higher than the other cell populations and had the most significant cellular heterogeneity, in which a distinct subcluster co-expressed endothelial markers. The transition trajectory of differentiation from smooth muscle cells into fibroblasts was depicted using the pseudotime analysis, suggesting that the expansion of corpus cavernosum is possibly compromised as a result of fibrosis. Cell-cell communications among ECs, smooth muscle cells, fibroblasts, and macrophages were robust, which indicated that inflammation may also have a crucial role in the development of ED.ConclusionsOur study has demonstrated a comprehensive single-cell atlas of cellular components in human corpus cavernosum of ED, providing in-depth insights into the pathogenesis. Future research is warranted to explore disease-specific alterations for individualized treatment of ED.

Background: Previous study has reported that loss of epithelial androgen receptor (AR) may promote tumor progression and cause TRAMP mouse model die earlier. The detail mechanisms, however, remain unclear. Methods: Immunohistochemistry assay, Western blot and real-time PCR were used to detect the expression of epithelial and mesenchymal markers. RNA extraction, RT-PCR, quantitative RT-PCR, BrdU incorporation assays, flow cytometry and other experimental technics were also used in present work. Results: Decreased expression of epithelial markers (Cytokeratin 8, NKX3.1 and E-cadherin) and increased expression of mesenchymal markers (α-SMA, Vimentin, and N-cadherin) in were found in AR knockout TRAMP tumors. Further investigation indicated that AR signal deprivation is associated with cell morphology transition, high cell mobility, high cell invasion rate and resistance to anoikis in TRAMP prostate tumor cells. Together, these findings implied knockout AR in TRAMP prostate tumor may lead to EMT, which may result in earlier metastasis, and then cause TRAMP mice die earlier. TGF-β1 is responsible for EMT in AR knockout TRAMP tumor cells. Conclusions: In conclusion, ADT therapy induced hormone refractory prostate cancer may gain the ability of metastasis through cell's EMT which is a phase of poor differentiation. Anti-EMT drugs should be developed to battle the tumor metastasis induced by ADT therapy.

Background: The long non-coding (lncRNA) RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is known to promote tumorigenesis, whereas microRNA-145 (miR-145) plays an antitumor role in several cancers. In this study, we aimed to elucidate the role of MALAT1 and miR-145 in prostate cancer cells and investigate the effect of MALAT1 downregulation on prostate cancer (PCa) cells in vitro in vivo.Methods: The Cancer Genome Atlas (TCGA) datasets were used to carry out the initial bioinformatics analysis; the findings were then tested in LNCaP and CWR22Rv1 cell lines. Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to evaluate the levels of MALAT1 and miR-145 along with related biomarkers. Furthermore, wound-healing and Transwell assays were performed to test the migratory and invasive abilities of PCa cells. Luciferase reporter assays were used to validate the relationship between MALAT1 and miR-145; their down-stream target genes were also studied. To further substantiate these findings in an animal model, tumor studies including immunofluorescence staining of tissues were carried in nude mice. Results: The expression of MALAT1 was upregulated in both LNCaP cell lines and CWR22Rv1 cell lines (F=2.882, t=13.370, P<0.001; F=2.268, t=15.859, P<0.001). Knockdown of MALAT1 reduced the migratory and invasive capabilities of PCa cells (F=0.017, t=12.212, P<0.001; F=10.723, t=6.016, P=0.002). Using direct binding, MALAT1 suppressed the antitumor function of miR-145, which in turn upregulated transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) via SMAD3 and TGFBR2 (F=2.097, t=5.389, P=0.006; F=1.306, t=4.155, P=0.014). Conclusions:We confirmed that MALAT1 acts as a competing endogenous RNA (ceRNA) of miR-145.The MALAT1 based regulation of MiR-145-5p-SMAD3/TGFBR2 interactions could be an intriguing molecular pathway for the progression of PCa.

Purpose As the mechanism of interaction between circular RNAs (circRNAs) and microRNAs (miRNAs) in regulating the development of prostate cancer (PCa) is not clear, this study focuses on investigating these effects. Materials and Methods Sample tissues were collected from the PCa of patients, and microarray analysis of human circRNAs was conducted. The expression of circ_0001686, hsa_miR-411-5p (miR-411-5p) were also detected by qRT-PCR. Circ_0001686 and miR-411-5p mimics were transfected into the PCa cell lines (CWR22RV1and LNCaP) and MTT, colony formation, Transwell, and scratch wound assays were used to analyze the biological behaviors of PCa cells. Si-circ_0001686 and ASO-miR-411-5p were used as negative controls, and dual-luciferase reporter assays were performed to verify the interactions among circ_0001686, miR-411-5p, and SMAD3/TGFBR2. The levels of SMAD3 and TGFBR2 in different treated PCa cells were measured by western blot, and in vivo experiments in a nude mouse model were carried out to strengthen the in vitro findings of miR-411-5p. Results The expression of circ_0001686 was up-regulated, while the expression of miR-411-5p was down-regulated in PCa cells. Moreover, circ_0001686 promoted cell proliferation, migration, and invasion. Molecular mechanism exploration revealed that circ_0001686 could reduce miR-411-5p, affecting the downstream target genes of SMAD3 and TGFBR2. In vitro and in vivo studies verified that miR-411-5p inhibits PCa progression. Conclusions Circ_0001686 can reduce miR-411-5p to increase the expression of SMAD3/TGFBR2, which consequently promotes the proliferation, invasion, and migration of PCa cells.

Background: This study aims to present the trends of incidence and mortality of kidney cancer from 1990 to 2016 by age, gender, geographical region, regional, and sociodemographic index (SDI), and then forecast the future trends to 2030.Methods: Data of this study were gathered from the Global Burden of Disease Study (GBD), including 195 countries and territories, accounting for 21 regions. Over-time trends from 1990 to 2016 were analyzed by gender, geographical region, age range and SDI. Based on the big data, we forecasted the future trends to 2030 by ARIMA model. All the data were analyzed by R software (x64 version 3.5.1), SAS (version 9.3) and SPSS (version 22.0).Results: Globally, in 2016, there were 342,100 [95% uncertainty interval (UI), 330,759-349,934] incident cases of kidney cancer and the number of deaths were 131,800 (127,185). The age-standardized incidence rate (ASIR) and death rate (ASDR) were 4.97 (4.81-5.09) per 100,000 and 2.00 (1.93-2.06) per 100,000, respectively. Globally, the estimated risk of kidney cancer for male within the age of 30 and 70 is around 0.79% compared to 0.41% for female. In other words, the probability of developing kidney cancer was generally higher in male than in female. By 2030, incidence of kidney cancer in both sexes are projected to increase substantially in high SDI, followed by middle SDI, low-middle SDI, and low SDI countries. High SDI and low SDI countries will also have increased mortality rates of kidney cancers. Globally, the trends in deaths due to kidney cancer will remain stable. Conclusions:The incidence and death rate of kidney cancer are highly variable among SDI countries and regions but have increased uniformly from 1990 to 2016. By 2030, the future incidence of kidney cancer will grow continuously especially in high SDI countries, middle SDI, low-middle SDI, and low SDI countries.

Background: This research aims to identify the current and future trends in the incidence and death rate of prostate cancer and to provide the necessary data support for making relevant health decisions.Methods: This study used the collected data and methodologies to describe the incidence and mortality trends of prostate cancer from 1990 to 2016. Based on the data, this paper projected the future trends in prostate cancer incidence and death rate.