scholarly journals Vitamin D receptor ligands, adenomatous polyposis coli, and the vitamin D receptor Fok I polymorphism collectively modulate β-catenin activity in colon cancer cells

2009 ◽  
Vol 49 (4) ◽  
pp. 337-352 ◽  
Author(s):  
Jan B. Egan ◽  
Patricia A. Thompson ◽  
Milen V. Vitanov ◽  
Leonid Bartik ◽  
Elizabeth T. Jacobs ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Vitamin D Receptor ◽  
Adenomatous Polyposis ◽  
Colon Cancer Cells ◽  
Polyposis Coli ◽  
Receptor Ligands

scholarly journals Genes regulating membrane-associated E-cadherin and proliferation in adenomatous polyposis coli mutant colon cancer cells: High content siRNA screen

PLoS ONE ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. e0240746
Author(s):  
Lauren E. King ◽  
Hui-Hua Zhang ◽  
Cathryn M. Gould ◽  
Daniel W. Thomas ◽  
Lachlan W. Whitehead ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Colon Cancer Cells ◽  
Polyposis Coli ◽  
Sirna Screen ◽  
Coli Mutant ◽  
E Cadherin

The effects of genistein and daidzein on cell proliferation kinetics in HT29 colon cancer cells: the expression of CTNNBIP1 (β-catenin), APC (adenomatous polyposis coli) and BIRC5 (survivin)

Human Cell ◽  
2014 ◽  
Vol 27 (2) ◽  
pp. 78-84 ◽  
Author(s):  
Sandra Regina Lepri ◽  
Leonardo Campos Zanelatto ◽  
Patrícia Benites Gonçalves da Silva ◽  
Daniele Sartori ◽  
Lucia Regina Ribeiro ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Colon Cancer Cells ◽  
Polyposis Coli ◽  
Proliferation Kinetics

scholarly journals Regulation of Wnt signaling by the tumor suppressor adenomatous polyposis coli does not require the ability to enter the nucleus or a particular cytoplasmic localization

2012 ◽  
Vol 23 (11) ◽  
pp. 2041-2056 ◽  
Author(s):  
David M. Roberts ◽  
Mira I. Pronobis ◽  
John S. Poulton ◽  
Eric G. Kane ◽  
Mark Peifer
Keyword(s):  
Colon Cancer ◽  
Tumor Suppressor ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Subcellular Location ◽  
Adenomatous Polyposis ◽  
Colon Cancer Cells ◽  
Polyposis Coli ◽  
Drosophila Embryos

Wnt signaling plays key roles in development and disease. The tumor suppressor adenomatous polyposis coli (APC) is an essential negative regulator of Wnt signaling. Its best-characterized role is as part of the destruction complex, targeting the Wnt effector β-catenin (βcat) for phosphorylation and ultimate destruction, but several studies suggested APC also may act in the nucleus at promoters of Wnt-responsive genes or to shuttle βcat out for destruction. Even in its role in the destruction complex, APC's mechanism of action remains mysterious. We have suggested APC positions the destruction complex at the appropriate subcellular location, facilitating βcat destruction. In this study, we directly tested APC's proposed roles in the nucleus or in precisely localizing the destruction complex by generating a series of APC2 variants to which we added tags relocalizing otherwise wild-type APC to different cytoplasmic locations. We tested these for function in human colon cancer cells and Drosophila embryos. Strikingly, all rescue Wnt regulation and down-regulate Wnt target genes in colon cancer cells, and most restore Wnt regulation in Drosophila embryos null for both fly APCs. These data suggest that APC2 does not have to shuttle into the nucleus or localize to a particular subcellular location to regulate Wnt signaling.

scholarly journals Original CIN: reviewing roles for APC in chromosome instability

2008 ◽  
Vol 181 (5) ◽  
pp. 719-726 ◽  
Author(s):  
Nasser M. Rusan ◽  
Mark Peifer
Keyword(s):  
Colon Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Adenomatous Polyposis Coli ◽  
Chromosome Instability ◽  
Original Sin ◽  
Adenomatous Polyposis ◽  
Colon Cancer Cells ◽  
Polyposis Coli ◽  
Bumper Sticker

You may have seen the bumper sticker “Eve was framed.” Thousands of years of being blamed for original sin and still many wonder, where's the evidence? Today, the tumor suppressor adenomatous polyposis coli (APC) may have the same complaint about accusations of a different type of CIN, chromosome instability. A series of recent papers, including three in this journal, propose that loss of APC function plays an important role in the CIN seen in many colon cancer cells. However, a closer look reveals a complex story that raises more questions than answers.

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