ArticleThe American journal of pathology2010
Desmosomal plakophilins in the prostate and prostatic adenocarcinomas: implications for diagnosis and tumor progression.
Article in The American journal of pathology, 2010. 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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Who cites it
27 citing papers in PubMed, 55 citations in OpenAlex.
- Urinary Extracellular Vesicle Signatures as Biomarkers in Prostate Cancer Patients.International journal of molecular sciences · 2025Article
- Plakophilin 1 in cancer: context-dependent dualism, subcellular dynamics, and therapeutic targeting.Frontiers in cell and developmental biology · 2025Review
- Role and function of plakophilin 3 in cancer progression and skin disease.Cancer science · 2024Review
- Comprehensive Analysis Identifies PKP3 Overexpression in Pancreatic Cancer Related to Unfavorable Prognosis.Biomedicines · 2023Article
- Disease-related blood-based differential methylation in cystic fibrosis and its representation in lung cancer revealed a regulatory locus inEpigenetics · 2022Article
- Identification of Novel Diagnostic Biomarkers in Prostate Adenocarcinoma Based on the Stromal-Immune Score and Analysis of the WGCNA and ceRNA Network.Disease markers · 2022Article
- Desmosomes as Signaling Hubs in the Regulation of Cell Behavior.Frontiers in cell and developmental biology · 2021Review
- Immune molecular profiling of a multiresistant primary prostate cancer with a neuroendocrine-like phenotype: a case report.BMC urology · 2020Article
- Desmoglein 1 Regulates Invadopodia by Suppressing EGFR/Erk Signaling in an Erbin-Dependent Manner.Molecular cancer research : MCR · 2019Article
- Increased expression of plakophilin 3 is associated with poor prognosis in ovarian cancer.Medicine · 2019Article
- Desmoglein-2 is overexpressed in non-small cell lung cancer tissues and its knockdown suppresses NSCLC growth by regulation of p27 and CDK2.Journal of cancer research and clinical oncology · 2017Article
- Plakophilin 1-deficient cells upregulate SPOCK1: implications for prostate cancer progression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Mice with Hepatic Loss of the Desmosomal Protein γ-Catenin Are Prone to Cholestatic Injury and Chemical Carcinogenesis.The American journal of pathology · 2015Article
- Desmosome regulation and signaling in disease.Cell and tissue research · 2015Review
- Desmosomes in acquired disease.Cell and tissue research · 2015Review
- Review
- Plakophilins 1 and 3 bind to FXR1 and thereby influence the mRNA stability of desmosomal proteins.Molecular and cellular biology · 2014Article
- Plakophilin-3 catenin associates with the ETV1/ER81 transcription factor to positively modulate gene activity.PloS one · 2014Article
- Mechanistic basis of desmosome-targeted diseases.Journal of molecular biology · 2013Review
- Plakophilin-associated RNA-binding proteins in prostate cancer and their implications in tumor progression and metastasis.Virchows Archiv : an international journal of pathology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The plakophilins, members of the armadillo-repeat family, consist of three different proteins (PKP1-3) that are specifically recruited to desmosomal plaques in a highly cell type-specific manner. Using immunofluorescence, immunoelectron microscopy, and immunoblot, we found that all three plakophilins occurred in luminal and basal cells of the pseudostratified prostate epithelium. The analysis of 135 cases of prostatic adenocarcinomas grouped into tumors with low (Gleason score < or = 6), intermediate (Gleason score 7), and high Gleason score (8 < or = Gleason score < or = 10) showed that the expression of PKP1 was reduced or lost in adenocarcinomas with high Gleason scores. The expression of PKP2 was unchanged in all prostatic adenocarcinomas analyzed. In contrast, PKP3 expression was increased in carcinomas with high Gleason scores in comparison with carcinomas with low Gleason scores. In DU 145 cell lines with either overexpression or knockdown of PKP3, both imbalances resulted in fewer desmosomal cell contacts. In addition, overexpression of PKP3 in DU 145 cells led to an augmentation in proliferation rate. Our data imply that both loss of PKP1 and up-regulation of PKP3 expression are biologically important events in prostate cancer and are associated with a more aggressive phenotype.
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