Regulation of metastasis of bladder cancer cells through the WNT signaling pathway

Du, Yueyao; Wang, Yongchuan; Zhang, Fei; Wu, Wenbo; Wang, Wei; Li, Hao; Xia, Shujie; Liu, Haitao

doi:10.1007/s13277-015-3563-3

Cited by 17 publications

(19 citation statements)

References 34 publications

(45 reference statements)

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“…58 Therefore, LiCl has been widely used as a surrogate compound to assess the involvement of the Wnt/β-catenin pathway. [59][60][61][62][63][64] Interestingly, the current knowledge of the Wnt pathway can now explain clinical observation made even before the Wnt pathways have been described. Early case reports already demonstrated that treatment of patients suffering from chronic schizophrenia and asthma with LiCl not only reduced the manic episodes but also caused a reduction of asthma attacks and the use of asthma-specific medication, 65 and other clinical observations showed that stopping a long-lasting LiCl therapy in a patient-induced increased airway hyper-responsiveness and asthma symptoms.…”

Section: Immunological Role Of Wnt Pathways In Asthmamentioning

confidence: 99%

Take the Wnt out of the inflammatory sails: modulatory effects of Wnt in airway diseases

Reuter

Beckert

Taube

2016

Laboratory Investigation

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Bronchial asthma and chronic obstructive pulmonary disease (COPD) are chronic diseases that are associated with inflammation and structural changes in the airways and lungs. Recent findings have implicated Wnt pathways in critically regulating inflammatory responses, especially in asthma. Furthermore, canonical and noncanonical Wnt pathways are involved in structural changes such as airway remodeling, goblet cell metaplasia, and airway smooth muscle (ASM) proliferation. In COPD, Wnt pathways are not only associated with structural changes in the airways but also involved in the development of emphysema. The present review summarizes the role and function of the canonical and noncanonical Wnt pathway with regard to airway inflammation and structural changes in asthma and COPD. Further identification of the role and function of different Wnt molecules and pathways could help to develop novel therapeutic options for these diseases.

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Section: Immunological Role Of Wnt Pathways In Asthmamentioning

confidence: 99%

Take the Wnt out of the inflammatory sails: modulatory effects of Wnt in airway diseases

Reuter

Beckert

Taube

2016

Laboratory Investigation

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“…Dickkopf-1 (DKK1), a transcriptional target of the Wnt/ β -catenin pathway, functions as a negative regulator of Wnt signaling [9]. It has been reported that Wnt signaling inhibition by DKK1 limits the invasiveness of various types of cancer and that pathway activation by lithium chloride normally promotes cancer cell metastasis [9–11]. Accordingly, the Wnt/ β -catenin signaling pathway is considered an important regulator of cancer cell metastasis; therefore, more in-depth researches of the mechanisms that regulate the Wnt/ β -catenin pathway may provide a new perspective for more effective TSCC therapies.…”

Section: Introductionmentioning

confidence: 99%

miR-373-3p Targets DKK1 to Promote EMT-Induced Metastasis via the Wnt/β-Catenin Pathway in Tongue Squamous Cell Carcinoma

Weng

Zhang

Wang

et al. 2017

BioMed Research International

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MicroRNAs (miRNAs) regulate gene expression and at the same time mediate tumorigenesis. miR-373-3p has diverse effects in tumors, but its role in tongue squamous cell carcinoma (TSCC) remains unknown. The purpose of this study is to determine the function of miR-373-3p in the progression of TSCC. Our results brought to light that miR-373-3p is markedly upregulated in clinical TSCC tissues compared with paired adjacent normal tissues and has significant correlation with a more aggressive TSCC phenotype in patients. Gain-of-function and loss-of-function studies revealed that ectopic miR-373-3p overexpression promoted the metastasis of TSCC cells. Notably, Wnt/β-catenin signaling was hyperactivated in TSCC cells overexpressing miR-373-3p, and this pathway was responsible for the epithelial-mesenchymal transition (EMT) induced by miR-373-3p. Furthermore, miR-373-3p directly targeted and suppressed Dickkopf-1 (DKK1), a negative regulator of the Wnt/β-catenin signaling cascade. These results demonstrate that, by directly targeting DKK1, miR-373-3p constitutively activated Wnt/β-catenin signaling, thus promoting the EMT-induced metastasis of TSCC. Taken together, our findings reveal a new regulatory mechanism for miR-373-3p and suggest that miR-373-3p might be a potential target in TSCC therapy.

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“…Here, miR-3713 is a novel number of the miRNA family and has not been reported of any direct targets, including MMP9. In our previous report, we have shown that MMP9 is a key regulator of TCC invasiveness, and the WNT signaling pathway seems to regulate TCC metastasis through activation of MMP912.…”

Section: Discussionmentioning

confidence: 94%

“…Nevertheless, the molecular pathway that regulates MMP9 activation has been shown to be different in different cancers. We recently reported that activation of WNT signaling pathway increased metastasis of TCC through activation of MMP912. However, the signal pathways to control MMP9 activation in TCC has not been completely clarified.…”

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confidence: 99%

MicroRNA-3713 regulates bladder cell invasion via MMP9

Wang

et al. 2016

Sci Rep

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Transitional cell carcinoma (TCC) is the most common type of bladder cancer but its carcinogenesis remains not completely elucidated. Dysregulation of microRNAs (miRNAs) is well known to be involved in the development of various cancers, including TCC, whereas a role of miR-3713 in the pathogenesis of TCC has not been appreciated. Here, we reported that significantly higher levels of matrix metallopeptidase 9 (MMP9), and significantly lower levels of miR-3713 were detected in TCC tissue, compared to the adjacent non-tumor tissue, and were inversely correlated. Moreover, the low miR-3713 levels in TCC specimens were associated with poor survival of the patients. In vitro, overexpression of miR-3713 significantly decreased cell invasion, and depletion of miR-3713 increased cell invasion in TCC cells. The effects of miR-3713 on TCC cell growth appeared to result from its modification of MMP9 levels, in which miR-3713 was found to bind to the 3′-UTR of MMP9 mRNA to inhibit its protein translation in TCC cells. This study highlights miR-3713 as a previously unrecognized factor that controls TCC invasiveness, which may be important for developing innovative therapeutic targets for TCC treatment.

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Regulation of metastasis of bladder cancer cells through the WNT signaling pathway

Cited by 17 publications

References 34 publications

Take the Wnt out of the inflammatory sails: modulatory effects of Wnt in airway diseases

Take the Wnt out of the inflammatory sails: modulatory effects of Wnt in airway diseases

miR-373-3p Targets DKK1 to Promote EMT-Induced Metastasis via the Wnt/β-Catenin Pathway in Tongue Squamous Cell Carcinoma

MicroRNA-3713 regulates bladder cell invasion via MMP9

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