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Beta-Catenin Expression
Published by Anonymous on 2007/9/29 (1788 reads)
1: Crit Rev Toxicol. 2005 Oct-Nov;35(8-9):727-38.


Mode of action: inhibition of histone deacetylase, altering WNT-dependent gene expression, and regulation of beta-catenin--developmental effects of valproic acid.

Wiltse J.

US Environmental Protection Agency, Washington, DC, USA. dpatton@ilsi.org

Valproic acid (VPA) has long been known to cause spina bifida, a neural tube defect, and other effects in fetuses of women treated with this drug. Toxicological tests in laboratory mice and rats at human therapeutic doses also show neural tube and other defects. Studies show that VPA alters Wnt signaling in human and animal cells, inducing Wnt-dependent gene expression at doses that cause developmental effects. Structural analogues of VPA that do not have this effect on Wnt signaling do not cause developmental effects. Similarly, Trichostatin A, a compound that mimics VPA in its effects on Wnt gene expression, also causes similar developmental effects. Alteration of Wnt signaling is empirically well supported as the postulated mode of action (MOA) for VPA's developmental effects in animals. VPA causes alteration of Wnt signaling in both human and animal cells systems at the same dose levels. The correspondence of effects on signaling and of effects on development in animals and humans supports the view that alteration of Wnt signaling is a relevant MOA in humans.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

PMID: 16417040 [PubMed - indexed for MEDLINE]

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2: Endocr Pathol. 2004 Winter;15(4):329-37.


beta-Catenin expression in thyroid follicular lesions: potential role in nuclear envelope changes in papillary carcinomas.

Rezk S, Brynes RK, Nelson V, Thein M, Patwardhan N, Fischer A, Khan A.

Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01655, USA.

The morphologic distinction of benign and malignant thyroid follicular lesions can sometimes be challenging, therefore an immunohistochemical marker to aid in this distinction would be useful. beta-Catenin is one such potential marker. It is part of a membrane-bound cell growth-signaling complex that plays a role in cell adhesion, as well as in promotion of growth through activation of the Wnt signaling pathway. Oncogenic signaling occurs when beta-catenin is released, accumulates in the cytoplasm, translocates into the nucleus, and promotes transcription of genes including bcl-1 (cyclin D1) and c-myc that induce cell proliferation. Paraffin blocks from 133 thyroidectomy specimens were stained with monoclonal antibodies reactive with beta-catenin and cyclin D1. These included 53 cases of papillary thyroid carcinoma (PTC), 46 cases of follicular variant of papillary carcinoma (FVPC), 10 cases of follicular carcinoma (FC), and 24 cases of follicular adenoma (FA). Tissue from six normal thyroid specimens served as a control. The malignant lesions (PTC, FC, and FVPC) expressed strong cytoplasmic/nuclear staining and minimal residual membranous staining in 87%, 80%, and 71% of cases, respectively. In contrast, all normal thyroid tissue and 79% of FAs showed strong membranous reactivity with very minimal cytoplasmic staining. Interestingly, in 83% of PTC cases and 20% FVPCs, the intranuclear inclusions were distinctly beta-catenin positive. Cyclin D1 over expression correlated with cytoplasmic relocalization of beta-catenin in almost all cases, and no evidence of cyclin D1 gene amplification was observed. beta-Catenin can be of a diagnostic utility for thyroid lesions, because it highlights intranuclear inclusions in PTC, and shifts from a membranous localization to a cytoplasmic localization in malignant lesions. We speculate that the localization of beta-catenin in intranuclear inclusions may reflect a cytoskeletal remodeling activity of beta-catenin that is functionally significant for the PTC pathway.

Publication Types:
Review

PMID: 15681857 [PubMed - indexed for MEDLINE]

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3: Biochim Biophys Acta. 2004 Apr 1;1691(1):1-15.


Regulation of E-cadherin expression and beta-catenin/Tcf transcriptional activity by the integrin-linked kinase.

Oloumi A, McPhee T, Dedhar S.

British Columbia Cancer Agency and Jack Bell Research Centre, University of British Columbia, Vancouver Hospital, 2660 Oak St. Vancouver, BC, Canada V6H 3Z6.

Integrin-linked kinase (ILK) is a serine/threonine protein kinase which interacts with the cytoplasmic domains of beta1 and beta3 integrins. ILK structure and its localization at the focal adhesion allows it not only to interact with different structural proteins, but also to mediate many different signalling pathways. Extracellular matrices (ECM) and growth factors each stimulate ILK signalling. Constitutive activation of ILK in epithelial cells results in oncogenic phenotypes such as disruption of cell extracellular matrix and cell to cell interactions, suppression of suspension-induced apoptosis, and induction of anchorage independent cell growth and cell cycle progression. More specifically, pathological overexpression of ILK results in down-regulation of E-cadherin expression, and nuclear accumulation of beta-catenin, leading to the subsequent activation of the beta-catenin/Tcf transcription complex, the downstream components of the Wnt signalling pathway. Here we review the data implicating ILK in the regulation of these two signalling pathways, and discuss recent novel insights into the molecular basis and requirement of ILK in the process of epithelial to mesenchymal transformation (EMT).

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 15053919 [PubMed - indexed for MEDLINE]

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4: Srp Arh Celok Lek. 2003 Jan-Feb;131(1-2):73-6.


[Adhesion molecules in Wilm's tumor: expression and significance of beta-catenin (part II)]

[Article in Serbian]

Basta-Jovanović G, Radojević S, Djuricić S, Savin M, Skodrić S, Bunjevacki G, Hadzi-Djokić J, Nesić V.

Institute of Pathology, University School of Medicine, Belgrade.

Beta-catenin is a glicoprotein which has an important role in cell-cell adhesion, as well as in cell signal transmission, in u regulation of gen expression and in interaction with axin and APC (adenomatous poliposis coli). Its oncogenic role in several types of carcinomas in human population is well known. It is very likely that beta-catenin as an protooncogen plays an important role in genesis of Wilms tumor. It is well known that in 15% Wilms tumors there are beta-catenin mutations, which indicates that there is a disorder in Wnt signal path that plays an important role in Wilms tumor genesis. The aim of our study was to investigate b-catenin expression in Wilms tumor, to compare it with the expression in normal renal tissue as well as to see if there is a positive correlation between b-catenin expression in Wilms tumor with tumor stage, histologic type and/or prognostic group.

Publication Types:
English Abstract
Review

PMID: 14608868 [PubMed - indexed for MEDLINE]

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5: Clin Colorectal Cancer. 2003 Aug;3(2):113-20.


Adenomatous polyposis coli/beta-catenin interaction and downstream targets: altered gene expression in gastrointestinal tumors.

Clements WM, Lowy AM, Groden J.

Howard Hughes Medical Institute, and Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

Gastrointestinal cancer affects 250,000 Americans a year with nearly half of those cases being colorectal cancer. The Wnt pathway is activated in most spontaneous and familial colorectal cancers and has been implicated in tumor formation at other sites in the gastrointestinal tract. In human tumors, the Wnt pathway is most often altered by mutations affecting certain components of this signal transduction cascade-the adenomatous polyposis coli (APC) tumor suppressor gene or the ss-catenin gene. Perturbations in the function of either protein lead to altered gene regulation through the interaction of ss-catenin with T-cell factor (Tcf)/lymphoid enhancer binding protein (Lef) transcription factors. This review will discuss the Wnt pathway, examine the mutations of its components that are found in human cancer, and discuss the known downstream gene targets.

Publication Types:
Review

PMID: 12952568 [PubMed - indexed for MEDLINE]

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6: EMBO Rep. 2000 Jul;1(1):24-8.


Curbing the nuclear activities of beta-catenin. Control over Wnt target gene expression.

Hecht A, Kemler R.

Max-Planck-Institute of Immunobiology, Freiburg, Germany. hecht@immunbio.mpg.de

Wnt molecules control numerous developmental processes by altering specific gene expression patterns, and deregulation of Wnt signaling can lead to cancer. Many Wnt factors employ beta-catenin as a nuclear effector. Upon Wnt stimulation, beta-catenin heterodimerizes with T-cell factor (TCF) DNA-binding proteins to form a transcriptional activator complex. As the activating subunit of this complex, beta-catenin performs dual tasks: it alleviates repression of target gene promoters and subsequently it activates them. Beta-catenin orchestrates these effects by recruiting chromatin modifying cofactors and contacting components of the basal transcription machinery. Although beta-catenin and TCFs are universal activators in Wnt signaling, their target genes display distinct temporal and spatial expression patterns. Apparently, post-translational modifications modulate the interactions between TCFs and beta-catenin or DNA, and certain transcription factors can sequester beta-catenin from TCFs while others synergize with beta-catenin-TCF complexes in a promoter-specific manner. These mechanisms provide points of intersection with other signaling pathways, and contribute to the complexity and specificity of Wnt target gene regulation.

Publication Types:
Review

PMID: 11256619 [PubMed - indexed for MEDLINE]

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7: Exp Cell Res. 2000 Nov 25;261(1):75-82.


The integration of cell adhesion with gene expression: the role of beta-catenin.

Ben-Ze'ev A, Shtutman M, Zhurinsky J.

Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, 76100, Israel. avri.ben-zeev@weizmann.ac.il

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 11082277 [PubMed - indexed for MEDLINE]

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8: Ann N Y Acad Sci. 1999;886:212-6.


Truncated form of beta-catenin and reduced expression of wild-type catenins feature HepG2 human liver cancer cells.

Carruba G, Cervello M, Miceli MD, Farruggio R, Notarbartolo M, Virruso L, Giannitrapani L, Gambino R, Montalto G, Castagnetta L.

Institute of Oncology, University of Palermo, Italy. lucashbl@unipa.it

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 10667222 [PubMed - indexed for MEDLINE]
 

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