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Transl Androl Urol ; 9(3): 1244-1251, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32676407


Background: The treatment of ketamine-induced bladder contractures remains poorly studied. We therefore evaluated the efficacy of cystectasia with a sodium hyaluronate balanced solution in this kind of bladder contracture. Methods: Eighteen patients presenting with ketamine-induced bladder contracture between July 2010 and February 2018 were selected and analysed. Ketamine was discontinued in all patients, who were then treated with weekly cystectasia (0.09% sodium hyaluronate balanced solution) 3 times. The volume of the first perfusion was twice the preoperatively measured bladder capacity, and the volume of the subsequent two perfusions was increased by 100 mL each time. The Pelvic Pain and Urgency/Frequency (PUF) symptom score, O'Leary-Sant Interstitial Cystitis (IC) Symptom Index (ICSI), IC Problem Index (ICPI), Quality of Life (QOL) score, and bladder capacity were recorded before surgery and 3 and 12 months after the 3rd expansion. Results: No significant complications were observed during the 3 expansions. Fourteen patients completed the full follow-up schedule. Preoperatively and at the 3- and 12-month follow-up evaluations performed after the 3rd expansion, the PUF symptom scores were 20.4±3.6, 11.5±3.1, and 13.2±3.3, respectively; the mean ICSI was 13.6±2.8, 7.7±2.3, and 8.2±2.5, respectively; the mean ICPI was 10.6±2.6, 7.3±2.1, and 7.7±2.5, respectively; and the mean QOL scores were 6.0±0, 2.1±0.5, and 2.7±0.8, respectively; and the mean bladder catheter volume was 83±27, 234±56, and 228±52 mL, respectively. There were significant differences between all preoperative and postoperative values. Conclusions: Cystectasia with a sodium hyaluronate balanced solution is an effective treatment modality for ketamine-induced bladder contracture.

Oncol Lett ; 14(6): 6888-6894, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29151918


In a previous study by the present authors, it was identified that the expression of engrailed-2 (EN2) gene was downregulated in clear cell renal cell carcinoma (cc-RCC). The aim of the present study was to determine whether aberrant methylation was the mechanism underlying the silencing of EN2 gene in cc-RCC. A total of forty paired cc-RCC tissues, four cc-RCC cell lines and one normal human proximal tubule epithelial cell line were evaluated for EN2 gene methylation status using methylation-specific polymerase chain reaction (PCR). Following treatment with 5-Aza-dc, reverse transcription-quantitative PCR and western blot analysis were performed to examine the expression of EN2. Furthermore, cell proliferation, apoptosis and invasion assays were conducted to analyze the inhibitory effects of EN2 re-expression in 786-O cells. The results of the present study demonstrated that hyper-methylation of EN2 was identified in 12/40 cc-RCC tissues and all cc-RCC cell lines. The methylation status of the EN2 gene was revealed to be associated with histological grade and tumor size in cc-RCC. Following 5-Aza-dc treatment, demethylation of the EN2 gene was identified in 786-O cells, in conjunction with EN2 re-expression. Furthermore, re-activation of the EN2 gene markedly inhibited the proliferative and invasive capacities of cc-RCC. The results of the present study demonstrated that the EN2 gene promoter was hyper-methylated in cc-RCC, which may underlie the silencing of the EN2 gene in cc-RCC.

J Mol Histol ; 47(3): 229-37, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-26948025


Our preliminary study indicated that Engrailed-2 (EN2) is downregulated but also ectopically expressed in clear-cell renal cell carcinoma (CCRCC), and the absence of EN2 expression was associated with poor histological grade. However, the specific roles of EN2 in CCRCC have yet to be elucidated. In the present study, we examined the effects of inhibiting EN2 expression by human renal tubular epithelial cells (HK-2) and overexpressing EN2 by human clear-cell renal cells (786-O). Results showed that EN2 inhibition accelerated HK-2 cell proliferation, shortened the cell cycle, reduced apoptosis, and acted more invasively. By contrast, EN2 overexpression in 786-O cells decelerated the proliferative ability of 786-O, increased the percentage of cell apoptosis, and weakened the invasive ability. Overall, the results demonstrated that EN2 might play an anti-oncogenic role in oncogenesis and development of CCRCC, thereby maintaining the normal growth of human renal tubular epithelial cells.

Carcinoma de Células Renais/metabolismo , Proteínas de Homeodomínio/metabolismo , Neoplasias Renais/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Apoptose/genética , Carcinoma de Células Renais/genética , Ciclo Celular/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Expressão Gênica , Proteínas de Homeodomínio/genética , Humanos , Neoplasias Renais/genética , Proteínas do Tecido Nervoso/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo
Asian Pac J Cancer Prev ; 16(11): 4665-9, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26107221


The aim of this study was to assess the diagnostic value of RASSF1A methylation in renal cell carcinoma. Systematically search were performed using the Pubmed, ProQest and Web of Science for all articles on the association between RASSF1A methylation and renal cell carcinoma before 15 April 2015. After the filtration, 13 studies involving 677 cases and 497 controls met our criteria. Our meta-analysis suggested that hypermethylation of RASSF1A gene was associated with the increased risk of RCC(OR:4.14, 95%CI:1.06-16.1). Stratified analyses showed a similar risk in qualitative detection method(OR:28.4, 95%CI:10.2-79.6), body fluid sample(OR:12.8, 95%CI:5.35-30.8), and American(OR:10.5, 95%CI:1.97-55.9). Our result identified that RASSF1A methylation had a strong potential in prediction the risk of Renal cell carcinoma.

Carcinoma de Células Renais/genética , Metilação de DNA , Predisposição Genética para Doença , Neoplasias Renais/genética , Regiões Promotoras Genéticas/genética , Proteínas Supressoras de Tumor/genética , Estudos de Casos e Controles , Humanos , Prognóstico , Fatores de Risco
Mol Biol Rep ; 41(6): 3651-7, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24532139


Engrailed-2 (EN2), a member of the homeobox family of genes, encodes a homeodomain-containing transcription factor that is thought to be a potential oncogene in a number of cancers. Because the role of EN2 in clear cell renal cell carcinoma (CCRCC) has not been determined, we investigated its expression in CCRCC tissues and cell lines. Using immunohistochemical (IHC) staining, we found that EN2 protein was expressed in normal renal cells and tubules, but was frequently down-regulated in tissues from patients with CCRCC and in CCRCC cell lines. In addition, we found that EN2, which functions in the nucleus, was completely localized to the cytoplasm of CCRCC cells as detected by IHC and immunofluorescence staining. Furthermore, expression of EN2 protein was negatively correlated with increasing histological grade of CCRCC tumors (P = 0.003). The exact role of EN2 expression in renal carcinoma carcinogenesis requires further investigation.

Carcinoma de Células Renais/genética , Proteínas de Homeodomínio/biossíntese , Neoplasias Renais/genética , Proteínas do Tecido Nervoso/biossíntese , Adulto , Idoso , Carcinoma de Células Renais/patologia , Feminino , Regulação Neoplásica da Expressão Gênica , Proteínas de Homeodomínio/genética , Humanos , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Proteínas do Tecido Nervoso/genética