The aim of the present study was to investigate risk-related microRNAs (miRs) for bladder urothelial carcinoma (BUC) prognosis. Clinical and microRNA expression data downloaded from the Cancer Genome Atlas were utilized for survival analysis. Risk factor estimation was performed using Cox's proportional regression analysis. A microRNA-regulated target gene network was constructed and presented using Cytoscape. In addition, the Database for Annotation, Visualization and Integrated Discovery was used for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment, followed by protein-protein interaction (PPI) network analysis. Finally, the K-clique method was applied to analyze sub-pathways. A total of 16 significant microRNAs, including hsa-miR-3622a and hsa-miR-29a, were identified (P<0.05). Following Cox's proportional regression analysis, hsa-miR-29a was screened as a prognostic marker of BUC risk (P=0.0449). A regulation network of hsa-miR-29a comprising 417 target genes was constructed. These target genes were primarily enriched in GO terms, including collagen fibril organization, extracellular matrix (ECM) organization and pathways, such as focal adhesion (P<0.05). A PPI network including 197 genes and 510 interactions, was constructed. The top 21 genes in the network module were enriched in GO terms, including collagen fibril organization and pathways, such as ECM receptor interaction (P<0.05). Finally, 4 sub-pathways of cysteine and methionine metabolism, including paths 00270_4, 00270_1, 00270_2 and 00270_5, were obtained (P<0.01) and identified to be enriched through DNA (cytosine-5)-methyltransferase (DNMT)3A, DNMT3B, methionine adenosyltransferase 2α (MAT2A) and spermine synthase (SMS). The identified microRNAs, particularly hsa-miR-29a and its 4 associated target genes DNMT3A, DNMT3B, MAT2A and SMS, may participate in the prognostic risk mechanism of BUC.

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Sirtuin 6 (SIRT6), a DNA repair-related gene, has undergone an extremely thorough study for its involvement in the development of many different cancers. The objective of our study was to explore the function and mechanism of SIRT6-induced regulation of prostate cancer (PCa). RT-PCR was performed to validate the levels of SIRT6 in PCa cell lines. Cell proliferation, migration, and invasion of cells with SIRT6 knockdown were assessed using CCK-8 assay, colony formation assay, wound-healing assay, and transwell assay. Western blot was applied to assess the related proteins. We found that SIRT6 expression was distinctly upregulated in PCa specimens and cells. Loss-of-functional assays revealed that SIRT6 silence suppressed the proliferation and metastasis of PCa cells. Mechanistic studies revealed that SIRT6 silence inhibited Wnt/β‐catenin signaling and EMT progress. Overall, the study confirmed the upregulation of SIRT6 in patients with PCa and its association with the progression. SIRT6 promoted PCa progression by regulating Wnt/β‐catenin signaling, providing a promising biomarker and treatment approach for preventing PCa.

Prostate cancer is a type of adenocarcinoma arising from the peripheral zone of the prostate gland, and metastasized prostate cancer is incurable with the current available therapies. The present study aimed to identify open chromosomal regions and differentially expressed genes (DEGs) associated with prostate cancer development. The DNase sequencing data (GSE33216) and RNA sequencing data (GSE22260) were downloaded from the Gene Expression Omnibus database. DNase I hypersensitive sites were detected and analyzed. Subsequently, DEGs were identified and their potential functions were enriched. Finally, upstream regulatory elements of DEGs were predicted. In LNCaP cells, following androgen receptor activation, 244 upregulated and 486 downregulated open chromosomal regions were identified. However, only 1% of the open chromosomal regions were dynamically altered. The 41 genes with upregulated open chromosomal signals within their promoter regions were primarily enriched in biological processes. Additionally, 211 upregulated and 150 downregulated DEGs were identified in prostate cancer, including eight transcription factors (TFs). Finally, nine regulatory elements associated with prostate cancer were predicted. In particular, inhibitor of DNA binding 1 HLH protein (ID1) was the only significantly upregulated TF which exhibited motif enrichment in the promoter regions of upregulated genes. CCCTC‑binding factor (CTCF) and ELK1 ETS transcription factor (ELK1), enriched in the open promoter regions of downregulated genes, were potential upstream regulatory elements. Furthermore, reverse transcription‑quantitative polymerase chain reaction analysis confirmed that ID1 expression was significantly upregulated in LNCaP cells and 5α‑dihydrotestosterone (DHT)‑treated LNCaP cells compared with that in BPH1 cells, while CTCF and ELK1 expression was significantly downregulated in LNCaP cells and DHT‑treated LNCaP cells. In conclusion, ID1, CTCF and ELK1 may be associated with prostate cancer, and may be potential therapeutic targets for the treatment of this disease.

MiR‐490‐3p is regarded as a tumor suppressor in many cancers, but whether miR‐490‐3p is involved in the development of bladder cancer remains unknown. BALB/c nude mice (male, 15–20 g) were used to investigate the role of MiR‐490‐3p in bladder cancer. The relationship between miR‐490‐3p and PCBP2 involved in bladder cancer regulation were determined. Cell viability, proliferation, and cell cycle were estimated by cell counting kit‐8 (CCK‐8) assay, 5‐bromo‐2′‐deoxyuridine (BrdU) detection, and flow cytometry analysis, respectively. In animal experiments, lentivirus was transfected into bladder cancer cells to overexpress miR‐490‐3p, which were then injected into mice and the change of tumor volume was assessed. Principal findings: The expression of MiR‐490‐3p was decreased in bladder cancer cells. Overexpression of miR‐490‐3p inhibited bladder cancer cell viability and proliferation. Moreover, overexpression of miR‐490‐3p caused cell cycle arrest in bladder cancer cells. The inhibitory effect of miR‐490‐3p on bladder cancer cells growth could be counteracted by enhancing PCBP2 expression. In vivo, bladder cancer growth in mice was blocked by miR‐490‐3p upregulation. MiR‐490‐3p suppressed bladder cancer growth and bladder cancer cell proliferation by down‐regulating PCBP2 expression.