This study aimed to investigate infiltration related microRNAs (miRNAs) in bladder urothelial carcinoma (BUC). Twenty patients with BUC were enrolled and divided into 2 groups according to infiltration or not: infiltrating BUC group (n=12) and non-infiltrating BUC group (n=8). Gene chip was used to detect infiltration related miRNAs in the BUC samples. In other recruited 17 patients with BUC who were divided into infiltrating BUC samples (n=14) and non-infiltrating BUC samples (n=3), and in 4 BUC cell lines (EJ, 5637, T24 and BIU-87), the expression of miRNAs was assayed by using reverse transcription-polymerase chain reaction (RT-PCR). In infiltrating BUC group, as compared with non-infiltrating BUC group, there were 7 differentially expressed miRNAs: hsa-miR-29c, hsa-miR-200a, hsa-miR-378, hsa-miR-429, hsa-miR-200c and hsa-miR-141 were up-regulated, while hsa-miR-451 was down-regulated. In the BUC samples, the results of RT-PCR were consistent with those by the miRNA array. In the cancer cell lines, RT-PCR in T24 only revealed the similar expression pattern of miRNAs to that by the miRNA array. It is suggested that infiltration of BUC is related with different expression of miRNAs, which may provide a novel platform for further study on function and action mechanism of miRNAs.
Carcinoma ; genetics ; Cell Line, Tumor ; Humans ; MicroRNAs ; genetics ; Urinary Bladder ; metabolism ; Urinary Bladder Neoplasms ; genetics

Xanthogranulomatous cystitis is a rare benign chronic inflammatory disease. To the best of our knowledge, only 16 cases have been reported in the literature. The etiology of xanthogranulomatous cystitis may include immunological disorders, abnormal lipid metabolism, a reduction of chemotactic activities, and metaplasia of the urothelium due to a chronic infection. Only one case has been reported in the Korean literature. Here we describe two cases of xanthogranulomatous cystitis with a review of the previous reports.
Cystitis* ; Inflammation ; Lipid Metabolism ; Metaplasia ; Urinary Bladder ; Urothelium

Diabetic bladder dysfunction (DBD) is a common complication in the lower urinary tract of diabetes. In recent years, mesenchymal stem cell (MSC) have broad application prospects in the treatment of DBD. MSC can migrate to damaged bladder tissue and differentiate into various cell types, such as urothelial cells, myofibroblasts, smooth muscle cells and nerve cells, promote bladder tissue repair and regeneration through paracrine effects. In addition, MSC also intervene in the pathological process of DBD, reverse disease progression, and restore partial bladder function through immune regulation, improvement of oxidative stress, and regulation of blood glucose. At present, the treatment of DBD with MSC is limited to preclinical animal experiments, clinical research and application should be pursued further.
Animals ; Urinary Bladder ; Mesenchymal Stem Cells ; Diabetes Mellitus/metabolism*

Resistance to anticancer chemotherapeutic drugs remains a major obstacle in cancer chemotherapy. A variety of mechanisms responsible for drug resistance has been posed. Mdr gene overexpression and detoxification by glutathione are believed to be involved in such mechanisms. Recently, we established two low-dose cisplatin-resistant human bladder cancer cell lines, T24RO.5 and T24R1, which showed resistance at O.5 hg/ml and 1 hg/ml of cisplatin, respectively. The resistance of T24RO.5 and T24R1 cells to cisplatin were 9.4 and 9.37 fold compared to that of the parental T24 cells In this study, we investigated the total glutathione content and p-glycoprotein expression, a mdr gene product, in parent and resistant cell lines to elucidate the drug resistance mechanism to cisplatin. Glutathione content was measured by biochemical method. P-glycoprotein expression was measured by flowcytometry using monoclonal antibody to p-glycoprotein. Glutathione content and p-glycoprotein expression were not different between parental and all resistant cell lines. These results suggest that mdr gene and glutathione do not play a role in cisplatin resistance mechanism in these low-dose cisplatin-resistant cell lines. Further work will be necessary to determine the mechanism of drug resistance in this model.
Cell Line* ; Cisplatin* ; Drug Resistance ; Drug Therapy ; Genes, MDR* ; Glutathione* ; Humans ; Metabolism* ; P-Glycoprotein ; Parents ; Urinary Bladder Neoplasms ; Urinary Bladder*

B7-H1, a recently described member of the B7 family of costimulatory molecules, is thought to be involved in tumor immune escape by inducing T-cell apoptosis. In order to investigate the relationship between B7-H1 and immune escape of bladder cancer, B7-H1 expression in 50 cases of bladder cancer was detected by using immunohistochemical method. Survival curves were constructed using the Kaplan-Meier method and independent prognostic factors were evaluated using the Cox regression model. Our results showed that the positive rate of B7-H1 immunostaining in normal bladder tissue and bladder cancer was 0 and 72% respectively. The expression of B7-H1 was strongly associated with the pathological grade, clinical stage and recurrence (P<0.05). The survival rate was significantly lower in patients with B7-H1 positive group than in those with B7-H1 negative group and multi-variable analysis revealed that B7-H1 could be regarded as an independent factor in evaluating the prognosis of bladder cancer. It is concluded that the expression of B7-H1 is strongly associated with neoplastic progression and prognosis of bladder cancer. The manipulation of B7-H1 may become a beneficial target for immunotherapy in human bladder cancer.
Antigens, CD/genetics ; Antigens, CD/*metabolism ; Antigens, CD80/genetics ; Antigens, CD80/*metabolism ; Prognosis ; Tumor Escape/*genetics ; Urinary Bladder Neoplasms/*immunology ; Urinary Bladder Neoplasms/metabolism

OBJECTIVE: To explore the molecular mechanism by which microRNA let-7g-3p regulates biological behaviors of bladder cancer cells. METHODS: The expression levels of let-7g-3p in bladder cancer and adjacent tissues, normal bladder epithelial cells (HUC cells) and bladder cancer cells (T24, 5637 and EJ cells) were detected using qRT- PCR. T24 cells were transfected with let-7g-3p mimic or inhibitor, and the changes in cell proliferation, migration, invasion, and apoptosis were examined. Transcriptome sequencing was carried out in cells overexpressing let-7g-3p, and the results of bioinformatics analysis, double luciferase reporter gene assay, qRT-PCR and Western blotting confirmed that HMGB2 gene was the target gene of let-7g-3p. The expression of HMGB2 was examined in HUC, T24, 5637 and EJ cells, and in cells with HMGB2 knockdown, the effect of let-7g-3p knockdown on the biological behaviors were observed. RESULTS: qRT-qPCR confirmed that let-7g-3p expression was significantly lower in bladder cancer tissues and cells (P < 0.01). Overexpression of let-7g-3p inhibited cell proliferation, migration and invasion, and promoted cell apoptosis, while let-7g-3p knock-down produced the opposite effects. Bioinformatics and transcriptome sequencing results showed that HMGB2 was the key molecule that mediate the effect of let-7g-3p on bladder cancer cells. Luciferase reporter gene assay, qRT-PCR and Western blotting all confirmed that HMGB2 was negatively regulated by let-7g-3p (P < 0.01). Knocking down HMGB2 could partially reverse the effect of let-7g-3p knockdown on the biological behaviors of the bladder cancer cells. CONCLUSION The microRNA let-7g-3p can inhibit the biological behavior of bladder cancer cells by negatively regulating HMGB2 gene.
Apoptosis ; Cell Line, Tumor ; Cell Movement/physiology* ; Cell Proliferation ; Epithelial Cells/metabolism* ; Gene Expression Regulation, Neoplastic ; HMGB2 Protein/metabolism* ; Humans ; MicroRNAs/metabolism* ; Urinary Bladder ; Urinary Bladder Neoplasms/genetics*

Antigens, CD20 ; metabolism ; Carcinoma in Situ ; classification ; diagnosis ; metabolism ; pathology ; Diagnosis, Differential ; Humans ; Hyaluronan Receptors ; metabolism ; Hyperplasia ; Precancerous Conditions ; diagnosis ; metabolism ; pathology ; Tumor Suppressor Protein p53 ; metabolism ; Urinary Bladder ; metabolism ; pathology ; Urinary Bladder Neoplasms ; classification ; diagnosis ; metabolism ; pathology ; Urothelium ; metabolism ; pathology

Actins ; metabolism ; Adult ; Female ; Humans ; Melanoma-Specific Antigens ; metabolism ; Microphthalmia-Associated Transcription Factor ; metabolism ; Perivascular Epithelioid Cell Neoplasms ; metabolism ; pathology ; surgery ; Urinary Bladder ; metabolism ; pathology ; surgery ; Urinary Bladder Neoplasms ; metabolism ; pathology ; surgery

OBJECTIVETo detect the expression of apoptosis gene PDCD5 in tissues of normal human kidney, renal clear cell carcinoma, normal bladder and bladder carcinoma, and explore the role of PDCD5 gene in renal clear cell carcinoma and bladder carcinoma.

METHODSIndirect immunohistochemistry was employed to detect PDCD5 expression in 63 kidney specimens and 42 bladder specimens. Positive expression rates and intensity of PDCD5 protein expression in the kidney tissue were investigated microscopically and by computerized image analysis. Positive expression rate in the bladder tissue was investigated by microscopic observation.

RESULTSThe results of immunohistochemical staining showed PDCD5 protein overexpression in the renal tubule of normal human kidney tissues and downregulation with the stage increase of renal clear cell carcinoma. PDCD5 protein expression showed statistical significance in tissues of normal kidney and renal clear cell carcinoma in all stages. No obvious PDCD5 expression was detected in the tissues of normal human bladder and bladder carcinoma.

CONCLUSIONPDCD5 is an important apoptosis-regulating factor in the occurrence of renal clear cell carcinoma, and its expression is extremely low in tissues of normal human bladder and bladder carcinoma.

Adult ; Aged ; Apoptosis Regulatory Proteins ; biosynthesis ; Carcinoma, Renal Cell ; metabolism ; Carcinoma, Transitional Cell ; metabolism ; Female ; Humans ; Immunohistochemistry ; Kidney ; metabolism ; Kidney Neoplasms ; metabolism ; Male ; Middle Aged ; Neoplasm Proteins ; biosynthesis ; Urinary Bladder ; metabolism ; Urinary Bladder Neoplasms ; metabolism

The 8-hydroxydeoxyguanosine (8-OH-dG), DNA adduct produced by oxygen radical-induced hydroxylation of C-8 position of guanine residue is accepted as to cause mutation and associate with carcinogenesis, and there are many carcinogens those produce oxygen radicals. Although many carcinogens have been accepted to induce bladder tumor, there is little known about the mechanism of carcinogenesis by these carcinogens. Following administration of bladder carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), 4-Aminobiphenyl (4-ABP), 2-naphthylamine (2-NA) and N-methyl-N-nitrosourea (MNU) to human normal bladder epithelial cell, the results were obtained.1. Following administration of aromatic amine carcinogen, BBN, 4-ABP and 2-NA, the content of 8-OH-dG was increased to about 30-35 % although some variation of time existed according to the kinds of carcinogens. 2. Following administration of MNU, the content of 8-OH-dG was increased to about less than 3 % over all times. 3. Following administration of H2O2 that produce oxygen radicals without metabolism, the content of 8-OH-dG was increased to about 37 %. From this result, it can be supposed that the in crease of 8-OH-dG by carcinogens is induced by oxygen radical.The results obtained suggest that there are some enzymes in bladder epithelium that are related to metabolism of aromatic amine carcinogens and modification of DNA in bladder epithelial cell by the oxygen radicals, that is Formation of 8-OH-dG, is induced in carcinogenesis of bladder tumor byaromatic amine carcinogens.
2-Naphthylamine ; Carcinogenesis ; Carcinogens* ; DNA* ; Epithelial Cells ; Epithelium ; Guanine ; Humans* ; Hydroxylation ; Metabolism ; Methylnitrosourea ; Oxygen ; Reactive Oxygen Species ; Urinary Bladder Neoplasms ; Urinary Bladder*