ArticleMolecular cancer2011
Protein kinase A antagonist inhibits β-catenin nuclear translocation, c-Myc and COX-2 expression and tumor promotion in Apc(Min/+) mice.
Article in Molecular cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 61 citations in OpenAlex.
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- G-Protein-Coupled Receptor 5 (LGR5) Overexpression Activates β-Catenin Signaling in Breast Cancer Cells via Protein Kinase A.Medical science monitor basic research · 2019Article
- Expression of Wnt-signaling pathway genes and their associations with miRNAs in colorectal cancer.Oncotarget · 2018Article
- Molecular genetics and targeted therapy of WNT-related human diseases (Review).International journal of molecular medicine · 2017Article
- Pharmacologic Manipulation of Wnt Signaling and Cancer Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2017Review
- Epac1 links prostaglandin E2 to β-catenin-dependent transcription during epithelial-to-mesenchymal transition.Oncotarget · 2016Article
- The Wnt signaling pathway in cancer.Critical reviews in oncology/hematology · 2016Review
- Molecular Mechanisms for cAMP-Mediated Immunoregulation in T cells - Role of Anchored Protein Kinase A Signaling Units.Frontiers in immunology · 2016Review
- Targeting the WNT Signaling Pathway in Cancer Therapeutics.The oncologist · 2015Review
- Bone marrow stroma-derived PGE2 protects BCP-ALL cells from DNA damage-induced p53 accumulation and cell death.Molecular cancer · 2015Article
- Prostaglandin E2 promotes MYCN non-amplified neuroblastoma cell survival via β-catenin stabilization.Journal of cellular and molecular medicine · 2015Article
- Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.The Journal of biological chemistry · 2014Article
- Protein kinase A activation enhances β-catenin transcriptional activity through nuclear localization to PML bodies.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe adenomatous polyposis coli (APC) protein is part of the destruction complex controlling proteosomal degradation of β-catenin and limiting its nuclear translocation, which is thought to play a gate-keeping role in colorectal cancer. The destruction complex is inhibited by Wnt-Frz and prostaglandin E(2) (PGE(2)) - PI-3 kinase pathways. Recent reports show that PGE(2)-induced phosphorylation of β-catenin by protein kinase A (PKA) increases nuclear translocation indicating two mechanisms of action of PGE(2) on β-catenin homeostasis.
findingsTreatment of Apc(Min/+) mice that spontaneously develop intestinal adenomas with a PKA antagonist (Rp-8-Br-cAMPS) selectively targeting only the latter pathway reduced tumor load, but not the number of adenomas. Immunohistochemical characterization of intestines from treated and control animals revealed that expression of β-catenin, β-catenin nuclear translocation and expression of the β-catenin target genes c-Myc and COX-2 were significantly down-regulated upon Rp-8-Br-cAMPS treatment. Parallel experiments in a human colon cancer cell line (HCT116) revealed that Rp-8-Br-cAMPS blocked PGE(2)-induced β-catenin phosphorylation and c-Myc upregulation.
conclusionBased on our findings we suggest that PGE(2) act through PKA to promote β-catenin nuclear translocation and tumor development in Apc(Min/+) mice in vivo, indicating that the direct regulatory effect of PKA on β-catenin nuclear translocation is operative in intestinal cancer.
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