Cited by 288Wnt/β-catenin signaling in development and cancerGenetic factors in colorectal cancerColorectal Cancer Treatments and Studies

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A Two-Step Model for Colon Adenoma Initiation and Progression Caused by APC Loss

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Phelps, Reid A., Chidester, Stephanie, Dehghanizadeh, Somaye, Phelps, Jason, Sandoval, Imelda T., Rai, Kunal, Broadbent, Talmage, Sarkar, Sharmistha, Burt, Randall W., Jones, David A.·2009·Cell

DOI 10.1016/j.cell.2009.02.037PMC PMC2706149

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Abstract

Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation. Using zebrafish and human cells, we show that homozygous loss of APC causes failed intestinal cell differentiation but that this occurs in the absence of nuclear beta-catenin and increased intestinal cell proliferation. Therefore, loss of APC is insufficient for causing beta-catenin nuclear localization. APC mutation-induced intestinal differentiation defects instead depend on the transcriptional corepressor C-terminal binding protein-1 (CtBP1), whereas proliferation defects and nuclear accumulation of beta-catenin require the additional activation of KRAS. These findings suggest that, following APC loss, CtBP1 contributes to adenoma initiation as a first step, whereas KRAS activation and beta-catenin nuclear localization promote adenoma progression to carcinomas as a second step. Consistent with this model, human FAP adenomas showed robust upregulation of CtBP1 in the absence of detectable nuclear beta-catenin, whereas nuclear beta-catenin was detected in carcinomas.

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Authors: Phelps, R. A., Chidester, S., Dehghanizadeh, S., Phelps, J., Sandoval, I. T., Rai, K., Broadbent, T., Sarkar, S., Burt, R. W., & Jones, D. A.
Affiliations: University of Utah (US)
Corresponding author: Jones, David A.
ORCID: Chidester, Stephanie
Dehghanizadeh, Somaye
Sandoval, Imelda T.
Rai, Kunal
Sarkar, Sharmistha
Jones, David A.
Venue: Cell
Publisher: Elsevier BV
Published: 2009-05
Volume: 137
Issue: 4
Pages: 623-634
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2009.02.037
PMC: PMC2706149
OpenAlex: W2018425992
Cited by: 286
References: 51
Citations by year: 2026: 2 · 2025: 3 · 2024: 5 · 2023: 9 · 2022: 8 · 2021: 13 · 2020: 11 · 2019: 14 · 2018: 14 · 2017: 18 · 2016: 22 · 2015: 23 · 2014: 17 · 2013: 23 · 2012: 28
FWCI: 13.97
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1538 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Huntsman Cancer Foundation
National Institutes of Health (5p01ca073992-15)
National Cancer Institute (R01CA116468, P01‐CA073992, CA96934, CA042014, CA073992, P30CA042014)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
Keywords: colonic adenoma, APC loss, Wnt/β-catenin signaling, β-catenin nuclear localization, CtBP1, KRAS activation, intestinal cell differentiation, intestinal cell proliferation, familial adenomatous polyposis, colorectal cancer, zebrafish
MeSH terms: Adenoma, Alcohol Oxidoreductases, Animals, Cell Differentiation, Colonic Neoplasms, DNA-Binding Proteins, Humans, Peptide Fragments, Adenomatous Polyposis Coli, Zebrafish, Signal Transduction, Gene Expression Regulation, Neoplastic, ras Proteins, Proto-Oncogene Proteins c-raf, rac1 GTP-Binding Protein, Adenomatous Polyposis Coli Protein, beta Catenin

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A Two-Step Model for Colon Adenoma Initiation and Progression Caused by APC Loss

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