Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Bryan, Richard T.

doi:10.1098/rstb.2014.0042

Cited by 59 publications

(48 citation statements)

References 135 publications

(298 reference statements)

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“…It is supposed that these dysregulated lncRNAs in different grade bladder cancer and normal urothelium may participate in biological processes of cancer [25][26][27][28]. Bryan RT1 et al found that N-and P-cadherin related to the cadherin cell adhesion and was the potential targets for the inhibition of cancer progression in bladder cancer [29]. Tomasetti et al proved DNA replication errors mutations were responsible for two-thirds of the mutations in human cancers by analyzing cancer genome sequencing and epidemiological data [30].…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Cao

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Bladder cancer (BC) is one of the most frequent urologic tumors worldwide. However, long non-coding RNA(lncRNA) expression profiles in BC progression remain unclear. This study aimed to explore lncRNA expression profiles in different grades of bladder cancer and normal urothelium tissues. Methods: We performed high-throughput sequencing in BC tissues of different grade and obtained the expression profiles of its lncRNAs. Then, aberrantly expressed lncRNAs were validated by quantitative reverse transcription polymerase chain reaction (RT-PCR). Gene Ontology (GO) and pathway analyses were used to investigate the potential function of these lncRNAs. Co-expresson network was constructed to explore the relationship between lncRNAs and target mRNAs. Results: We identified 252 aberrantly expressed lncRNAs in high-grade BC while compared to low-grade BC, and 269 lncRNAs in high-grade BC while compared to normal urothelium. Notably, we found 33 overlapped lncRNAs. Subsequently, 7 lncRNAs were selected from the overlapped part and confirmed by RT-PCR. GO and pathway analyses showed that these dysregulated lncRNAs participated in cell migration, cell adhesion, as well as Ras signaling pathway. Co-expression network and The Cancer Genome Atlas (TCGA) data showed LUCAT1 and CCNB1 had positive relationship in regulating the progress of bladder cancer. Conclusion: Our findings revealed the significant role of lncRNAs in the development process of bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Cao

Zhou

et al. 2018

Cell Physiol Biochem

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“…In an environment of degradation and destabilization of cell-cell adhesion and decreased E-cadherin expression, β-catenin is released into the cytoplasm causing it to accumulate and eventually lead to nuclear translocation (25). Cadherin switching is a hallmark of EMT, where E-cadherin can be replaced by an abnormal expression of N-cadherin without changes in E-cadherin levels (26). This event may be affected by cytokines and growth factors (27).…”

Section: Discussionmentioning

confidence: 99%

Effect of epithelial growth factor on matrix metalloproteinase-2 and E-cadherin/β-catenin expression in an in situ model of tumorigenesis

et al. 2017

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Abstract. The aim of the present study was to analyze the in vitro effect of various doses of epidermal growth factor (EGF; 5 and 10 ng/ml) on matrix metalloproteinase-2 (MMP-2) secretion and E-cadherin/β-catenin expression by co-cultured cells that mimic an in situ carcinoma ex-pleomorphic adenoma, where benign myoepithelial cells from a pleomorphic adenoma surround malignant epithelial cells. EGF was supplemented in various doses and the effects were evaluated following four days of cell culture. ELISA was performed to determine MMP-2 secretion levels. Gene expression for E-cadherin and β-catenin was analyzed using quantitative polymerase chain reaction. The results revealed that E-cadherin expression decreased when the cells were supplemented with 5 ng/ml EGF. ELISA results indicated that MMP-2 secretion increased when EGF was supplemented at concentrations of 5 and 10 ng/ml. The present findings demonstrated that EGF may be involved in the epithelial-mesenchymal transition process via altering the E-cadherin/β-catenin complex and increasing MMP-2 secretion, which may then favor the dissolution of the basement membrane to the benefit of malignant cell clusters, contributing to the development of an invasive phenotype in this in vitro model of tumorigenesis.

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“…In addition, activation of WNT signaling cascade by tumor cells owing to decreased E-cadherin levels, loss of β-catenin expression, its nuclear translocation and increased transcriptional activity have been examined to be associated with epithelial plasticity of tumor cells, disease aggression and metastasis formation. One of the serious implications of cadherin switching include the development of cancer stem cell phenotype and this makes the cadherin cell adhesion molecules and associated pathways, the probable target candidates for inhibition of cancer progression [16] . Tumor stroma/microenvironment has been shown to regulate tumor behavior by maintaining UroCSC population, its properties and EMT.…”

Section: Urothelial Cancer Stem Cells and Epithelial Plasticitymentioning

confidence: 99%

Epithelial plasticity in urothelial carcinoma: Current advancements and future challenges

Garg¹

2016

WJSC

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Urothelial carcinoma (UC) of the bladder is characterized by high recurrence rate where a subset of these cells undergoes transition to deadly muscle invasive disease and later metastasizes. Urothelial cancer stem cells (UroCSCs), a tumor subpopulation derived from transformation of urothelial stem cells, are responsible for heterogeneous tumor formation and resistance to systemic treatment in UC of the bladder. Although the precise reason for pathophysiologic spread of tumor is not clear, transcriptome analysis of microdissected cancer cells expressing multiple progenitor/stem cell markers validates the upregulation of genes that derive epithelial-to-mesenchymal transition. Experimental studies on human bladder cancer xenografts describe the mechanistic functions and regulation of epithelial plasticity for its cancer-restraining effects. It has been further examined to be associated with the recruitment of a pool of UroCSCs into cell division in response to damages induced by adjuvant therapies. This paper also discusses the various probable therapeutic approaches to attenuate the progressive manifestation of chemoresistance by co-administration of inhibitors of epithelial plasticity and chemotherapeutic drugs by abrogating the early tumor repopulation as well as killing differentiated cancer cells. Core tip: A subset of bladder cancer cells, known as urothelial cancer stem cells, have abilities to self-renew, generate tumor heterogeneity via differentiation, and are actually responsible for tumor relapse and metastasis formation. Delineating the mechanistic complexity between epithelial plasticity and cancer stemness in malignant transformation of urothelial carcinoma provides the basis for designing rational therapies. Differentiation and elimination therapies targeting the potential biomarkers could prove to be clinically beneficial by suppressing the cancer stemness and inhibiting epithelial-to-mesenchymal transition phenotype and would provide novel opportunities for targeted therapeutic approaches in the clinical management of patients.

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Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Cited by 59 publications

References 135 publications

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Effect of epithelial growth factor on matrix metalloproteinase-2 and E-cadherin/β-catenin expression in an in situ model of tumorigenesis

Epithelial plasticity in urothelial carcinoma: Current advancements and future challenges

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