ArticleJournal of cellular biochemistry2008
Beta-catenin mediates alteration in cell proliferation, motility and invasion of prostate cancer cells by differential expression of E-cadherin and protein kinase D1.
Article in Journal of cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Trichostatin A augments cell migration and epithelial-mesenchymal transition in esophageal squamous cell carcinoma throughWorld journal of gastroenterology · 2025Article
- Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling.Frontiers in oncology · 2022Review
- FK506 binding protein 10: a key actor of collagen crosslinking in clear cell renal cell carcinoma.Aging · 2021Article
- Attenuation of Tumor Suppressive Function of FBXO16 Ubiquitin Ligase Activates Wnt Signaling In Glioblastoma.Neoplasia (New York, N.Y.) · 2019Article
- Low Molecular Weight Mannogalactofucans Derived from Undaria pinnatifida Induce Apoptotic Death of Human Prostate Cancer Cells In Vitro and In Vivo.Marine biotechnology (New York, N.Y.) · 2018Article
- Cell line modeling to study biomarker panel in prostate cancer.The Prostate · 2016Article
- Knockdown of Upregulated Gene 11 (URG11) Inhibits Proliferation, Invasion, and β-Catenin Expression in Non-Small Cell Lung Cancer Cells.Oncology research · 2016Article
- Expression Level of Genes Coding for Cell Adhesion Molecules of Cadherin Group in Colorectal Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- From cell membrane to the nucleus: an emerging role of E-cadherin in gene transcriptional regulation.Journal of cellular and molecular medicine · 2014Review
- Protein kinase D1 attenuates tumorigenesis in colon cancer by modulating β-catenin/T cell factor activity.Oncotarget · 2014Article
- Delineation of the key aspects in the regulation of epithelial monolayer formation.Molecular and cellular biology · 2013Article
- Novel 3D co-culture model for epithelial-stromal cells interaction in prostate cancer.PloS one · 2013Article
- Diagnostic impact of promoter methylation and E-cadherin gene and protein expression levels in laryngeal carcinoma.Contemporary oncology (Poznan, Poland) · 2013Article
- PKD2 and PKD3 promote prostate cancer cell invasion by modulating NF-κB- and HDAC1-mediated expression and activation of uPA.Journal of cell science · 2012Article
- Curcumin attenuates β-catenin signaling in prostate cancer cells through activation of protein kinase D1.PloS one · 2012Article
- Emerging roles of protein kinase D1 in cancer.Molecular cancer research : MCR · 2011Review
- Ultraviolet activation of PKD: implications for skin cancer.Future oncology (London, England) · 2011Article
- Protein kinase D as a potential new target for cancer therapy.Biochimica et biophysica acta · 2010Review
- Article
- Effect of artemisinin derivatives on apoptosis and cell cycle in prostate cancer cells.Anti-cancer drugs · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that Protein Kinase D1 (PKD1) interacts with E-cadherin and is associated with altered cell aggregation and motility in prostate cancer (PC). Because both PKD1 and E-cadherin are known to be dysregulated in PC, in this study we investigated the functional consequences of combined dysregulation of PKD1 and E-cadherin using a panel of human PC cell lines. Gain and loss of function studies were carried out by either transfecting PC cells with full-length E-cadherin and/or PKD1 cDNA or by protein silencing by siRNAs, respectively. We studied major malignant phenotypic characteristics including cell proliferation, motility, and invasion at the cellular level, which were corroborated with appropriate changes in representative molecular markers. Down regulation or ectopic expression of either E-cadherin or PKD1 significantly increased or decreased cell proliferation, motility, and invasion, respectively, and combined down regulation cumulatively influenced the effects. Loss of PKD1 or E-cadherin expression was associated with increased expression of the pro-survival molecular markers survivin, beta-catenin, cyclin-D, and c-myc, whereas overexpression of PKD1 and/or E-cadherin resulted in an increase of caspases. The inhibitory effect of PKD1 and E-cadherin on cell proliferation was rescued by coexpression with beta-catenin, suggesting that beta-catenin mediates the effect of proliferation by PKD1 and E-cadherin. This study establishes the functional significance of combined dysregulation of PKD1 and E-cadherin in PC and that their effect on cell growth is mediated by beta-catenin.
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Registered trials
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.