The Bcl-w promoter is activated by β-catenin/TCF4 in human colorectal carcinoma cells

Lapham, Abigail; Adams, Jemimah E.; Paterson, Alex; Lee, Melanie; Brimmell, Matthew; Packham, Graham

doi:10.1016/j.gene.2008.12.002

Cited by 26 publications

(20 citation statements)

References 32 publications

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“…Additionally it is known that β-catenin regulates the expression of anti-apoptotic genes, e.g. survivin [30] as well as anti-apoptotic members of the Bcl- family [31]. We have found that depletion of β-catenin results in reduced expression of the anti-apoptotic proteins Mcl-1 and Bcl-xl showing the relevance of β-catenin for cell survival of metastatic melanoma cells.…”

Section: Discussionmentioning

confidence: 76%

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

et al. 2011

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Beta-catenin plays an important role in embryogenesis and carcinogenesis by controlling either cadherin-mediated cell adhesion or transcriptional activation of target gene expression. In many types of cancers nuclear translocation of beta-catenin has been observed. Our data indicate that during melanoma progression an increased dependency on the transcriptional function of beta-catenin takes place. Blockade of beta-catenin in metastatic melanoma cell lines efficiently induces apoptosis, inhibits proliferation, migration and invasion in monolayer and 3-dimensional skin reconstructs and decreases chemoresistance. In addition, subcutaneous melanoma growth in SCID mice was almost completely inhibited by an inducible beta-catenin knockdown. In contrast, the survival of benign melanocytes and primary melanoma cell lines was less affected by beta-catenin depletion. However, enhanced expression of beta-catenin in primary melanoma cell lines increased invasive capacity in vitro and tumor growth in the SCID mouse model. These data suggest that beta-catenin is an essential survival factor for metastatic melanoma cells, whereas it is dispensable for the survival of benign melanocytes and primary, non-invasive melanoma cells. Furthermore, beta-catenin increases tumorigenicity of primary melanoma cell lines. The differential requirements for beta-catenin signaling in aggressive melanoma versus benign melanocytic cells make beta-catenin a possible new target in melanoma therapy.

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Section: Discussionmentioning

confidence: 76%

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

et al. 2011

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“…A recent study suggests that the Wnt signalling results in increased apoptosis via increased expression of the proapoptotic factors bok and bax [24]. However, Wnt signalling also induces antiapoptotic factors bcl-W and bcl-2 expression [25, 26]. Since both pro- and antiapoptotic factors are upregulated in adenomas, tumour progression is likely caused by a balance between these factors.…”

Section: Discussionmentioning

confidence: 99%

Expression Profiling of Proliferation and Apoptotic Markers along the Adenoma-Carcinoma Sequence in Familial Adenomatous Polyposis Patients

Wang

El-Masry

Talbot

et al. 2013

Gastroenterology Research and Practice

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Introduction. Familial adenomatous polyposis (FAP) patients have a germline mutation in the adenomatous polyposis coli (APC) gene. The APC protein interacts with beta-catenin, resulting in the activation of the Wnt signalling pathway. This results in alterations in cell proliferation and apoptosis. We investigated the expression of beta-catenin and related proliferation and apoptotic factors in FAP patients, exploring the expression along the adenoma-carcinoma sequence. Methods. The expression of beta-catenin, p53, bcl-2, cyclin-D1, caspase-3, CD10, and Ki-67 proteins was studied by immunohistochemistry in samples of colonic nonneoplastic mucosa (n = 71), adenomas (n = 152), and adenocarcinomas (n = 19) from each of the16 FAP patients. Results. The expression of beta-catenin, caspase-3, cyclin-D1, and Ki-67 was increased in both adenomas and carcinomas in FAP patients, compared with normal mucosa. p53 and CD10 expression was only slightly increased in adenomas, but more frequently expressed in carcinomas. Bcl-2 expression was increased in adenomas, but decreased in carcinomas. Conclusion. This is the first study investigating collectively the expression of these molecules together in nonneoplastic mucosa, adenomas, and carcinomas from FAP patients. We find that beta-catenin and related proliferative and apoptotic factors (cyclin-D1, bcl-2, caspase-3, and Ki-67) are expressed early in the sequence, in adenomas. However, p53 and CD10 are often expressed later in the sequence, in carcinomas.

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“…It is known that the Wnt/ -catenin pathway activates transcription factors, such as TCF/LEF that are involved with proliferation and diVerentiation in colorectal cancer (Lapham et al 2009). Thus, we monitored the phosphorylation status of GSK-3 , a downstream protein target of Akt (Nakayama et al 2009), and observed a decrease in its phosphorylated state after PI3K inhibition (Fig.…”

Section: Pi3k Inhibition Interferes With Akt and Gsk-3 Activities Andmentioning

confidence: 99%

PI3K/Akt and GSK-3β prevents in a differential fashion the malignant phenotype of colorectal cancer cells

Araújo

Vidal

Souza

et al. 2010

J Cancer Res Clin Oncol

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The Bcl-w promoter is activated by β-catenin/TCF4 in human colorectal carcinoma cells

Cited by 26 publications

References 32 publications

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

Expression Profiling of Proliferation and Apoptotic Markers along the Adenoma-Carcinoma Sequence in Familial Adenomatous Polyposis Patients

PI3K/Akt and GSK-3β prevents in a differential fashion the malignant phenotype of colorectal cancer cells

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