Expression of E-cadherin and nm23 is associated with the clinicopathological factors of human non-small cell lung cancer in China

Chen, Xiaofeng; Zhang, Hong Tao; Qi, Qing-Yuan; Sun, Maomin; Tao, Luyang

doi:10.1016/j.lungcan.2004.09.009

Cited by 18 publications

(16 citation statements)

References 20 publications

(32 reference statements)

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“…For re-ChIP assays, immunoprecipitates were sequentially washed. Complexes were eluted by incubation with 10 mmol/L dithiothreitol (DTT) at 37 C for 30 minutes, diluted 50 times with dilution buffer (17), and then followed by a second immunoprecipitation with the indicated antibodies. Extracted DNA was analyzed by PCR using primers spanning the proximal promoter regions of CDH1 (nucleotide positions À276/À95), ABCG2 (À1250/À1050), or CASP3 (À456/À276).…”

Section: Chip and Re-chip Assaysmentioning

confidence: 99%

Diverse Targets of β-Catenin during the Epithelial–Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

Chang

Hsiao

et al. 2015

Cancer Research

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Wnt signaling contributes to the reprogramming and maintenance of cancer stem cell (CSC) states that are activated by epithelial-mesenchymal transition (EMT). However, the mechanistic relationship between EMT and the Wnt pathway in CSC is not entirely clear. Chromatin immunoprecipitation with highthroughput sequencing (ChIP-seq) indicated that EMT induces a switch from the b-catenin/E-cadherin/Sox15 complex to the b-catenin/Twist1/TCF4 complex, the latter of which then binds to CSC-related gene promoters. Tandem coimmunoprecipitation and re-ChIP experiments with epithelial-type cells further revealed that Sox15 associates with the b-catenin/E-cadherin complex, which then binds to the proximal promoter region of CASP3. Through this mechanism, Twist1 cleavage is triggered to regulate a b-catenin-elicited promotion of the CSC phenotype. During EMT, we documented that Twist1 binding to b-catenin enhanced the transcriptional activity of the b-catenin/TCF4 complex, including by binding to the proximal promoter region of ABCG2, a CSC marker.

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Section: Chip and Re-chip Assaysmentioning

confidence: 99%

Diverse Targets of β-Catenin during the Epithelial–Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

Chang

Hsiao

et al. 2015

Cancer Research

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“…We chose to focus on Nm23 for several reasons, the first of which being that, in a variety of different cancers, a decrease in both Nm23 and cadherin-mediated adhesion is observed, whereas the genes encoding these proteins remain unaltered (Chen et al, 2005;Che et al, 2006). Previous studies have also shown that Nm23 is both targeted by and regulates c-myc, which was the first identified target of the Wnt/b-catenin signaling network (He et al, 1998;Schuldiner et al, 2002;Arnaud-Dabernat et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Plakoglobin interacts with and increases the protein levels of metastasis suppressor Nm23-H2 and regulates the expression of Nm23-H1

et al. 2010

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Plakoglobin (c-catenin) is a homolog of b-catenin with similar dual adhesive and signaling functions. The adhesive function of these proteins is mediated by their interactions with cadherins, whereas their signaling activity is regulated by association with various intracellular partners. In this respect, b-catenin has a well-defined oncogenic activity through its role in the Wnt signaling pathway, whereas plakoglobin acts as a tumor/metastasis suppressor through mechanisms that remain unclear. We previously expressed plakoglobin in SCC9 squamous carcinoma cells (SCC9-P) and observed a mesenchymalto-epidermoid transition. Comparison of the protein and RNA profiles of parental SCC9 cells and SCC9-P transfectants identified various differentially expressed proteins and transcripts, including the nonmetastatic protein 23 (Nm23). In this study, we show that Nm23-H1 mRNA and Nm23-H2 protein are increased after plakoglobin expression. Coimmunoprecipitation and confocal microscopy studies using SCC9-P and various epithelial cell lines with endogenous plakoglobin expression revealed that Nm23 interacts with plakoglobin, cadherins and a-catenin. Furthermore, Nm23-H2 is the primary isoform involved in these interactions, which occur prominently in the cytoskeleton-associated pool of cellular proteins. In addition, we show that plakoglobinNm23 interaction requires the N-terminal (a-catenin interacting) domain of plakoglobin. Our data suggest that by increasing the expression and stability of Nm23, plakoglobin has a role in regulating the metastasis suppressor activity of Nm23, which may further provide a potential mechanism for the tumor/metastasis suppressor function of plakoglobin itself.

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“…59 EMT and loss of E-cadherin expression is also associated with disease progression, increased malignancy and poor prognosis in many epithelial tumors, including those of the colon, stomach, lung, bladder, oesophagus, prostate and breast. [60][61][62][63][64][65][66] Along with increased invasive properties, one of the key outcomes of EMT is a marked reduction in a cell's susceptibility to pro-apototic stimuli such as loss of cell-cell contact, growth factor withdrawal, and TNF-α. 39,67 Activation of transcription from the E-cadherin promoter is driven by ubiquitously expressed, and constitutively active transcription factors.…”

Section: Repression Of the Epithelial Phenotypementioning

confidence: 99%

C-terminal binding proteins: Emerging roles in cell survival and tumorigenesis

Bergman

Blaydes

2006

Apoptosis

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Expression of E-cadherin and nm23 is associated with the clinicopathological factors of human non-small cell lung cancer in China

Cited by 18 publications

References 20 publications

Diverse Targets of β-Catenin during the Epithelial–Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

Diverse Targets of β-Catenin during the Epithelial–Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

Plakoglobin interacts with and increases the protein levels of metastasis suppressor Nm23-H2 and regulates the expression of Nm23-H1

C-terminal binding proteins: Emerging roles in cell survival and tumorigenesis

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