ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Angiomotin is a novel component of cadherin-11/β-catenin/p120 complex and is critical for cadherin-11-mediated cell migration.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. 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.
- PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.Molecular and cellular biochemistry · 2025Article
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
- Tankyrase inhibition interferes with junction remodeling, induces leakiness, and disturbs YAP1/TAZ signaling in the endothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Determining the minimal amount of DMSO necessary to stabilize the Angiomotin lipid binding domain.Indiana University journal of undergraduate research · 2024Article
- Review
- GATA3 mediates nonclassical β-catenin signaling in skeletal cell fate determination and ectopic chondrogenesis.Science advances · 2022Article
- Advancement and properties of circular RNAs in prostate cancer: An emerging and compelling frontier for discovering.International journal of biological sciences · 2021Review
- Role of Tricellular Tight Junction Protein Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Cancer Cells.International journal of molecular sciences · 2019Review
- Review
- How many cadherins do human endothelial cells express?Cellular and molecular life sciences : CMLS · 2019Review
- Angiomotin-p130 inhibits β-catenin stability by competing with Axin for binding to tankyrase in breast cancer.Cell death & disease · 2019Article
- Combined overexpression of cadherin 6, cadherin 11 and cluster of differentiation 44 is associated with lymph node metastasis and poor prognosis in oral squamous cell carcinoma.Oncology letters · 2018Article
- The physiological role of Motin family and its dysregulation in tumorigenesis.Journal of translational medicine · 2018Review
- The role of cadherin-11 in microcystin-LR-induced migration and invasion in colorectal carcinoma cells.Oncology letters · 2018Article
- Using the Predicted Structure of the Amot Coiled Coil Homology Domain to Understand Lipid Binding.Indiana University journal of undergraduate research · 2018Article
- Positive regulation of TAZ expression by EBV-LMP1 contributes to cell proliferation and epithelial-mesenchymal transition in nasopharyngeal carcinoma.Oncotarget · 2017Article
- Should I stay or should I go? Cadherin function and regulation in the neural crest.Genesis (New York, N.Y. : 2000) · 2017Review
- Angiomotin regulates prostate cancer cell proliferation by signaling through the Hippo-YAP pathway.Oncotarget · 2017Article
- RNA-seq transcriptome analysis of formalin fixed, paraffin-embedded canine meningioma.PloS one · 2017Article
- Angiomotin Family Members: Oncogenes or Tumor Suppressors?International journal of biological sciences · 2017Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Loss of E-cadherin and up-regulation of mesenchymal cadherins, a hallmark of the epithelial-mesenchymal transition, contributes to migration and dissemination of cancer cells. Expression of human cadherin-11 (Cad11), also known as osteoblast cadherin, in prostate cancer increases the migration of prostate cancer cells. How Cad11 mediates cell migration is unknown. Using the human Cad11 cytoplasmic domain in pulldown assays, we identified human angiomotin (Amot), known to be involved in cell polarity, migration, and Hippo pathway, as a component of the Cad11 protein complex. Deletion analysis showed that the last C-terminal 10 amino acids in Cad11 cytoplasmic domain are required for Amot binding. Further, Cad11 preferentially interacts with Amot-p80 than Amot-p130 isoform and binds directly to the middle domain of Amot-p80. Cad11-Amot interaction affects Cad11-mediated cell migration, but not homophilic adhesion, as deletion of Amot binding motif of Cad11 (Cad11-ΔAmot) did not abolish Cad11-mediated cell-cell adhesion of mouse L cells, but significantly reduced Cad11-mediated cell migration of human C4-2B4 and PC3-mm2 prostate cancer cells and human HEK293T cells. Together, our studies identified Amot-p80 as a novel component of the Cad11 complex and demonstrated that Amot-p80 is critical for Cad11-mediated cell migration.
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