ArticlePloS one2013
Functional comparison of human adenomatous polyposis coli (APC) and APC-like in targeting beta-catenin for degradation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Seventeen primary malignant neoplasms involving the skin, ovary, esophagus, colon, oral cavity, and ear canal: a case report and review of the literature.Clinical journal of gastroenterology · 2021Review
- Mutations and mechanisms of WNT pathway tumour suppressors in cancer.Nature reviews. Cancer · 2021Review
- The 15-Amino Acid Repeat Region of Adenomatous Polyposis Coli Is Intrinsically Disordered and Retains Conformational Flexibility upon Binding β-Catenin.Biochemistry · 2020Article
- Branched actin networks are assembled on microtubules by adenomatous polyposis coli for targeted membrane protrusion.The Journal of cell biology · 2020Article
- WNT Signaling and Bone: Lessons From Skeletal Dysplasias and Disorders.Frontiers in endocrinology · 2020Review
- Bi-allelic Loss of Human APC2, Encoding Adenomatous Polyposis Coli Protein 2, Leads to Lissencephaly, Subcortical Heterotopia, and Global Developmental Delay.American journal of human genetics · 2019Article
- APC2 is critical for ovarian WNT signalling control, fertility and tumour suppression.BMC cancer · 2019Article
- Subtle Deregulation of the Wnt-Signaling Pathway Through Loss of Apc2 Reduces the Fitness of Intestinal Stem Cells.Stem cells (Dayton, Ohio) · 2018Article
- Hypermethylation of APC2 Is a Predictive Epigenetic Biomarker for Chinese Colorectal Cancer.Disease markers · 2018Article
- lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/β-catenin signaling.Nature medicine · 2017Article
- Induction of miR-3648 Upon ER Stress and Its Regulatory Role in Cell Proliferation.International journal of molecular sciences · 2017Article
- Functional redundancy between Apc and Apc2 regulates tissue homeostasis and prevents tumorigenesis in murine mammary epithelium.Oncogene · 2017Article
- Chemoprevention of intestinal tumorigenesis by the natural dietary flavonoid myricetin in APCMin/+ mice.Oncotarget · 2016Article
- The Poly(ADP-ribose) Polymerase Enzyme Tankyrase Antagonizes Activity of the β-Catenin Destruction Complex through ADP-ribosylation of Axin and APC2.The Journal of biological chemistry · 2016Article
- Naringin, a natural dietary compound, prevents intestinal tumorigenesis in Apc (Min/+) mouse model.Journal of cancer research and clinical oncology · 2016Article
- The two SAMP repeats and their phosphorylation state in Drosophila Adenomatous polyposis coli-2 play mechanistically distinct roles in negatively regulating Wnt signaling.Molecular biology of the cell · 2015Article
- Phospholipid remodeling and eicosanoid signaling in colon cancer cells.Indian journal of biochemistry & biophysics · 2014Review
- Self-association of the APC tumor suppressor is required for the assembly, stability, and activity of the Wnt signaling destruction complex.Molecular biology of the cell · 2014Article
- Testing models of the APC tumor suppressor/β-catenin interaction reshapes our view of the destruction complex in Wnt signaling.Genetics · 2014Article
- different Roles for the axin interactions with the SAMP versus the second twenty amino acid repeat of adenomatous polyposis coli.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Truncating mutations affect the adenomatous polyposis coli (APC) gene in most cases of colon cancer, resulting in the stabilization of β-catenin and uncontrolled cell proliferation. We show here that colon cancer cell lines express also the paralog APC-like (APCL or APC2). RNA interference revealed that it controls the level and/or the activity of β-catenin, but it is less efficient and binds less well to β-catenin than APC, thereby providing one explanation as to why the gene is not mutated in colon cancer. A further comparison indicates that APCL down-regulates the β-catenin level despite the lack of the 15R region known to be important in APC. To understand this discrepancy, we performed immunoprecipitation experiments that revealed that phosphorylated β-catenin displays a preference for binding to the 15 amino acid repeats (15R) rather than the first 20 amino acid repeat of APC. This suggests that the 15R region constitutes a gate connecting the steps of β-catenin phosphorylation and subsequent ubiquitination/degradation. Using RNA interference and domain swapping experiments, we show that APCL benefits from the 15R of truncated APC to target β-catenin for degradation, in a process likely involving heterodimerization of the two partners. Our data suggest that the functional complementation of APCL by APC constitutes a substantial facet of tumour development, because the truncating mutations of APC in colorectal tumours from familial adenomatous polyposis (FAP) patients are almost always selected for the retention of at least one 15R.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.