The canonical Wnt signalling pathway and its APC partner in colon cancer development

Schneikert, Jean; Behrens, Jürgen

doi:10.1136/gut.2006.093310

Cited by 261 publications

(233 citation statements)

References 95 publications

(70 reference statements)

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“…Wnt regulation of microRNAs in colorectal cancer T Schepeler et al notably malignancies of the large intestine due to the high frequency of mutations of Wnt signaling components (Schneikert and Behrens, 2007). So far, studies linking miRNAs to Wnt signaling in various contexts have only investigated a limited number of miRNAs because of predefined hypotheses relating to specific miRNAs (Martello et al, 2007;Kapinas et al, 2009) or a limited capacity (o100 miRNAs) of the analytical platform utilized .…”

Section: Discussionmentioning

confidence: 99%

Attenuation of the beta-catenin/TCF4 complex in colorectal cancer cells induces several growth-suppressive microRNAs that target cancer promoting genes

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Attenuation of the beta-catenin/TCF4 complex in colorectal cancer cells induces several growth-suppressive microRNAs that target cancer promoting genes

et al. 2011

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“…1a) (17,18) . Phosphorylated β-catenin is recognised by β-transducin repeat-containing protein which targets β-catenin for ubiquitination by the E3 ubiquitin ligase complex and, consequently, proteasomal degradation (16,18) .…”

Section: Proceedings Of the Nutrition Societymentioning

confidence: 99%

Is resistant starch protective against colorectal cancer via modulation of the WNT signalling pathway?

2015

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Epidemiological and experimental evidence suggests that non-digestible carbohydrates (NDC) including resistant starch are protective against colorectal cancer. These anti-neoplastic effects are presumed to result from the production of the SCFA, butyrate, by colonic fermentation, which binds to the G-protein-coupled receptor GPR43 to regulate inflammation and other cancer-related processes. The WNT pathway is central to the maintenance of homeostasis within the large bowel through regulation of processes such as cell proliferation and migration and is frequently aberrantly hyperactivated in colorectal cancers. Abnormal WNT signalling can lead to irregular crypt cell proliferation that favours a hyperproliferative state. Butyrate has been shown to modulate the WNT pathway positively, affecting functional outcomes such as apoptosis and proliferation. Butyrate's ability to regulate gene expression results from epigenetic mechanisms, including its role as a histone deacetylase inhibitor and through modulating DNA methylation and the expression of microRNA. We conclude that genetic and epigenetic modulation of the WNT signalling pathway may be an important mechanism through which butyrate from fermentation of resistant starch and other NDC exert their chemoprotective effects.

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“…In a small proportion of cases (B10%), activated mutations of the b-catenin gene (CTNNB1) are found (Schneikert and Behrens, 2007). However, recent findings revealed that Wnt ligands or inhibitors could affect the growth and survival of colon cancer cells in spite of the presence of APC or CTNNB1 mutations (Bafico et al, 2004;Suzuki et al, 2004;He et al, 2005).…”

mentioning

confidence: 98%

“…It is well known that the canonical Wnt signalling pathway is activated in most sporadic colorectal cancers (CRCs; B80%), which is mainly caused by mutations in the adenomatous polyposis coli (APC) gene (Segditsas and Tomlinson, 2006;Schneikert and Behrens, 2007). In a small proportion of cases (B10%), activated mutations of the b-catenin gene (CTNNB1) are found (Schneikert and Behrens, 2007).…”

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confidence: 99%

Down-regulation of frizzled-7 expression decreases survival, invasion and metastatic capabilities of colon cancer cells

et al. 2009

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BACKGROUND: The canonical Wnt signalling pathway is activated in most sporadic colorectal cancers (CRCs). We previously reported that FZD7 functions as a receptor for the canonical Wnt signalling pathway in colon cancer cells. METHODS AND RESULTS: In this study, we examined the function of FZD7 in survival, invasion and metastatic capabilities of colon cancer cells. FZD7_siRNA transfection decreased cell viability of HT-29 and HCT-116 colon cancer cells. Expression of c-Jun, phosphorylation of JNK and c-Jun, and activation of RhoA were suppressed after FZD7_siRNA transfection into HCT-116 cells. In vitro invasion activity and Wnt target gene expression were also reduced in HCT-116 cells transfected with FZD7_siRNA. Liver metastasis of stable FZD7_siRNA HCT-116 cell transfectants in scid mice was decreased to 40 -50% compared to controls. The mRNA levels of FZD7 in 135 primary CRC tissues were examined by real-time PCR. FZD7 mRNA levels were significantly higher in stage II, III or IV tumours than in non-tumour tissues (Po0.005), and overall survival was shorter in those patients with higher FZD7 expression (Po0.001). CONCLUSION: These data suggest that FZD7 may be involved in enhancement of survival, invasion and metastatic capabilities of colon cancer cells through non-canonical Wnt signalling pathways as well as the canonical pathway.

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The canonical Wnt signalling pathway and its APC partner in colon cancer development

Cited by 261 publications

References 95 publications

Attenuation of the beta-catenin/TCF4 complex in colorectal cancer cells induces several growth-suppressive microRNAs that target cancer promoting genes

Attenuation of the beta-catenin/TCF4 complex in colorectal cancer cells induces several growth-suppressive microRNAs that target cancer promoting genes

Is resistant starch protective against colorectal cancer via modulation of the WNT signalling pathway?

Down-regulation of frizzled-7 expression decreases survival, invasion and metastatic capabilities of colon cancer cells

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