β-Catenin/Wnt Signaling Regulates Expression of the Membrane Type 3 Matrix Metalloproteinase in Gastric Cancer

Lowy, Andrew M.; Clements, Wilson M.; Bishop, John W.; Kong, Ling; Bonney, Tera; Sisco, Karena; Aronow, Bruce J.; Fenoglio‐Preiser, Cecilia M.; Groden, Joanna

doi:10.1158/0008-5472.can-05-4268

Cited by 98 publications

(95 citation statements)

References 25 publications

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“…These results suggest that EMMPRIN-mediated regulation of b-catenin signaling is independent of MMP regulation and perhaps MMP expression is downstream of the Wnt/b-catenin signaling pathway. However, we cannot exclude the possibility that b-catenin signaling and MMP induction are stimulated independently through two distinct and separate pathways, although there is evidence that MMP expression can be stimulated by Wnt signaling (Roth et al, 2000;Soon et al, 2003;Lowy et al, 2006).…”

Section: Discussionmentioning

confidence: 95%

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

et al. 2010

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Advances in the field of tumor biology have identified that tumor cells co-opt developmental signaling pathways of embryonic stem cells and thus gain the ability to proliferate, differentiate and alter cell-cell interactions. One such pathway is the Wnt/b-catenin signaling pathway. High levels of EMMPRIN expression have been shown to correlate with poor prognosis and metastasis in a broad range of tumors. Although a variety of functions are attributed to EMMPRIN in tumorigenesis, the specific mechanism(s) through which it can exert its effects have not been elucidated, until now. In this study, we identify EMMPRIN as a novel regulator of the canonical Wnt/ b-catenin signaling pathway in lung cancer. Increasing EMMPRIN expression levels in lung cancer epithelial cells upregulated the b-catenin signaling pathway and silencing EMMPRIN inhibited b-catenin signaling, cell migration, proliferation, anchorage-independent growth and tumor growth in a mouse tumor xenograft model. These results provide a compelling rationale for targeting EMMPRIN for anticancer therapies. Understanding the molecular mechanisms driving EMMPRIN-induced lung tumorigenesis will provide enormous benefits in developing new therapeutic treatments for this and other forms of cancer.

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Section: Discussionmentioning

confidence: 95%

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

et al. 2010

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“…On the other hand, nuclear b-catenin is correlated with an invasive phenotype in intestinal-type tumors [198] . This increase in tumor invasion is likely mediated by the upregulation of Wnt transcriptional targets, such as EphA2 (erythropoietin-producing hepatocellular) and membrane type 3 matrix metalloproteinase (MT3-MMP) genes [199,200] . Furthermore, evidence provided by Kim et al [201,202] suggests that TC1 (C8orf4), which is upregulated in high-grade gastric cancers, coordinates the upregulation of Wnt/b-catenin target genes involved in the aggressive biological behavior and poor clinical outcome observed in advanced gastric cancer [202,203] .…”

Section: Wnt/b-catenin Signaling and Metastatic Potential In Gastric mentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

261

219

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Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput "omics" approaches will help in the search for Wnt pathway antagonist in the near future.

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“…Once the degradation of h-catenin is repressed (e.g., inhibition of GSK3h kinase activity), h-catenin accumulation results in its translocation into the nucleus and interaction with Tcf/LEF family transcription factors to activate the expression of target genes important for cell proliferation, such as c-myc and cyclin D1 (28). The h-catenin -dependent oncogenic signaling network is involved in the multistep process of tumorigenesis, including cell proliferation (29), invasion (30), and inhibition of apoptosis (31). The results in our study showed that the inhibition of CacyBP/SIP protein increased the expression of h-catenin without a change in the mRNA level in gastric cancer cells, suggesting that CacyBP/SIP may be a critical component required in the h-catenin ubiquitin-degradation pathway.…”

Section: The Expression Of B-catenin In Transfectantsmentioning

confidence: 99%

Calcyclin-Binding Protein Inhibits Proliferation, Tumorigenicity, and Invasion of Gastric Cancer

Ning¹,

Sun

Li³

et al. 2007

Molecular Cancer Research

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Calcyclin-binding protein/Siah-1 -interacting protein (CacyBP/SIP), a target protein of the S100 family, which includes S100A6, S100A1, S100A12, S100B, and S100P, has been identified as a component of a novel ubiquitinylation complex leading to B-catenin degradation. However, the function of CacyBP/SIP in gastric cancer has not been elucidated. In the present study, we prepared CacyBP/SIP overexpressing and knockdown cell lines of gastric cancer. Forced CacyBP/SIP expression inhibited the proliferation of gastric cancer cells, suppressed tumorigenicity in vitro, and prolonged the survival time of tumor-bearing nude mice. In addition, increased CacyBP/SIP repressed the invasive potential of gastric cancer cells. Conversely, the down-regulation of CacyBP/SIP by RNA interference showed the opposite effects. Further studies showed that depressed CacyBP/SIP increased the expression of total and nuclear B-catenin at the protein level and elevated the transcriptional activity of Tcf/LEF. Taken together, our results suggest that CacyBP/SIP may be a potential inhibitor of cell growth and invasion in the gastric cancer cell, at least in part through the effect on B-catenin protein expression and transcriptional activation of Tcf/LEF.

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β-Catenin/Wnt Signaling Regulates Expression of the Membrane Type 3 Matrix Metalloproteinase in Gastric Cancer

Cited by 98 publications

References 25 publications

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Calcyclin-Binding Protein Inhibits Proliferation, Tumorigenicity, and Invasion of Gastric Cancer

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