Downregulation of Dicer, a component of the microRNA machinery, in bladder cancer

Wu, Donghai; Tao, Jun; Xu, Bingying; Li, Pengchao; Lü, Qiang; Zhang, Wei

doi:10.3892/mmr.2011.711

Cited by 14 publications

(8 citation statements)

References 30 publications

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“…The discovery that miR are involved in neoplastic transformation attracted several scholars, and the number of scientific reports identifying new miR in carcinogenesis is increasing steadily. As expected, both miR [228], and Dicer (one of the proteins responsible for their maturation) [229] are involved in urologic cancers. Interestingly, the role of miR on gene expression depends upon their expression itself, which may be regulated either genetically or epigenetically [225, 230, 231], increasing the level of complexity of this mechanism of gene control.…”

Section: Epigenetic Changes In Bc: the Role Of Small Non-coding Rnas supporting

confidence: 54%

Bladder Cancer: A Simple Model Becomes Complex

Pierro

Gulìa

Cristini

et al. 2012

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Bladder cancer is one of the most frequent malignancies in developed countries and it is also characterized by a high number of recurrences. Despite this, several authors in the past reported that only two altered molecular pathways may genetically explain all cases of bladder cancer: one involving the FGFR3 gene, and the other involving the TP53 gene. Mutations in any of these two genes are usually predictive of the malignancy final outcome. This cancer may also be further classified as low-grade tumors, which is always papillary and in most cases superficial, and high-grade tumors, not necessarily papillary and often invasive. This simple way of considering this pathology has strongly changed in the last few years, with the development of genome-wide studies on expression profiling and the discovery of small non-coding RNA affecting gene expression. An easy search in the OMIM (On-line Mendelian Inheritance in Man) database using “bladder cancer” as a query reveals that genes in some way connected to this pathology are approximately 150, and some authors report that altered gene expression (up- or down-regulation) in this disease may involve up to 500 coding sequences for low-grade tumors and up to 2300 for high-grade tumors. In many clinical cases, mutations inside the coding sequences of the above mentioned two genes were not found, but their expression changed; this indicates that also epigenetic modifications may play an important role in its development. Indeed, several reports were published about genome-wide methylation in these neoplastic tissues, and an increasing number of small non-coding RNA are either up- or down-regulated in bladder cancer, indicating that impaired gene expression may also pass through these metabolic pathways. Taken together, these data reveal that bladder cancer is far to be considered a simple model of malignancy. In the present review, we summarize recent progress in the genome-wide analysis of bladder cancer, and analyse non-genetic, genetic and epigenetic factors causing extensive gene mis-regulation in malignant cells.

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Section: Epigenetic Changes In Bc: the Role Of Small Non-coding Rnas supporting

confidence: 54%

Bladder Cancer: A Simple Model Becomes Complex

Pierro

Gulìa

Cristini

et al. 2012

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“…Antibodies and dilutions used in immunocytochemistry were as follows: rabbit anti-PTEN (1:100); rabbit anti-RASSF1 (1:100); rabbit anti- PIK3R1 (1:100); rabbit anti IgG (1:400). The integrated optical density (IOD) was calculated for each sample [40]. For semi-quantitative analysis of the degree of staining, slides were independently scored by two pathologists.…”

Section: Methodsmentioning

confidence: 99%

Accumulated promoter methylation as a potential biomarker for esophageal cancer

Peng

Xue

et al. 2016

Oncotarget

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We performed a two-stage molecular epidemiological study to explore DNA methylation profiles for potential biomarkers of esophageal squamous cell carcinoma (ESCC) in a Chinese population. Infinium Methylation 450K BeadChip was used to identify genes with differentially methylated CpG sites. Sixteen candidate genes were validated by sequencing 1160 CpG sites in their promoter regions using the Illumina MiSeq platform. When excluding sites with negative changes, 10 genes (BNIP3, BRCA1, CCND1, CDKN2A, HTATIP2, ITGAV, NFKB1, PIK3R1, PRDM16 and PTX3) showed significantly different methylation levels among cancer lesions, remote normal-appearing tissues, and healthy controls. PRDM16 had the highest diagnostic value with the AUC (95% CI) of 0.988 (0.965–1.000), followed by PIK3R1, with the AUC (95% CI) of 0.969 (0.928–1.000). In addition, the methylation status was higher in patients with advanced cancer stages. These results indicate that aberrant DNA methylation may be a potential biomarker for the diagnosis of ESCC.

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“…It is worth to note that DICER and DROSHA play the crucial role in carcinogenesis. Accumulated evidences have shown that imbalance DICER and DROSHA expression levels are associated with bladder cancer risk [21-23]. Recently, Han and his colleagues also found that DICER and DROSHA expression levels were up-regulated in bladder cancer tissues compared to the matched normal bladder tissues, and silencing DICER or DROSHA can inhibit cell proliferation and induce cell apoptosis [24].…”

Section: Introductionmentioning

confidence: 99%

Genetic Variation in DROSHA 3’UTR Regulated by hsa-miR-27b Is Associated with Bladder Cancer Risk

et al. 2013

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PurposemiRNAs can regulate the biological processes, including differentiation, proliferation and apoptosis. DICER and DROSHA are two members of RNase III family, playing pivotal roles in the pathway of miRNAs biogenesis. In this study, we hypothesized that genetic variations of the DICER and DROSHA genes were associated with the bladder cancer risk.Experimental DesignWe performed a case-control study of 685 bladder cancer cases and 730 controls to investigate the association between the seven functional SNPs of DICER and DROSHA genes and bladder cancer risk. We then evaluated the functionality of the important SNPs.ResultsWe found that rs10719T>C polymorphism located in 3’ untranslated region (UTR) of DROSHA gene was associated with the increased risk of bladder cancer. Stratified analysis suggested that rs10719TC/CC genotype can increase risk of bladder cancer among male patients (Adjusted OR = 1.34, 95% CI = 1.05-1.70, P = 0.018), and ever smokers (1.56, 1.14-2.14, 0.006), compared with TT genotype. Furthermore, DROSHA rs10719T>C polymorphism was predicted to regulate the binding activity of hsa-miR-27a/b. Luciferase reported gene assay confirmed that rs10719 T to G substitution disrupted the binding site for hsa-miR-27b, resulting the increased levels of DROSHA protein.ConclusionsTaken together, these findings suggested that DROSHA rs10719T>C polymorphism may be associated with bladder cancer risk in a Chinese population, and hsa-miR-27b can influence the expression of DROSHA protein by binding with 3’UTR.

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Downregulation of Dicer, a component of the microRNA machinery, in bladder cancer

Cited by 14 publications

References 30 publications

Bladder Cancer: A Simple Model Becomes Complex

Bladder Cancer: A Simple Model Becomes Complex

Accumulated promoter methylation as a potential biomarker for esophageal cancer

Genetic Variation in DROSHA 3’UTR Regulated by hsa-miR-27b Is Associated with Bladder Cancer Risk

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