ArticleCancer medicine2015
PI3K/AKT pathway regulates E-cadherin and Desmoglein 2 in aggressive prostate cancer.
Article in Cancer medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Coupled Cell-Intrinsic and Microenvironmental Heterogeneity Drives Divergent Trajectories in Castration-Resistant Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- Desmoglein 2 is associated with dihydroartemisinin resistance in HeLa cervical cancer cells: a potential link to the PI3K/AKT signaling pathway.Discover oncology · 2026Article
- M1 Macrophage Extracellular Vesicles and TLR3 Agonist Nanoparticles Down-Regulate Immunosuppression and Metastasis via AKT/TAM in Triple-Negative Breast Cancer.Molecular carcinogenesis · 2025Article
- Eurycomanone Blocks TGF-β1-Induced Epithelial-to-Mesenchymal Transition, Migration, and Invasion Pathways in Human Non-Small Cell Lung Cancer Cells by Targeting Smad and Non-Smad Signaling.International journal of molecular sciences · 2025Article
- Biomarkers for Prostate Cancer Aggressiveness in Puerto Rican Men: Analysis of Phospho-Rb S249, N-cadherin, β-catenin, and E-cadherin Expression in Prostate Biopsies.Ponce Health Sciences University scientific journal · 2025Article
- Combretastatin A-4 suppresses the invasive and metastatic behavior of glioma cells and induces apoptosis in them: in-vitro study.Medical oncology (Northwood, London, England) · 2023Article
- Desmoglein-2 as a cancer modulator: friend or foe?Frontiers in oncology · 2023Review
- Harnessing conserved signaling and metabolic pathways to enhance the maturation of functional engineered tissues.NPJ Regenerative medicine · 2022Review
- Tracking Prostate Carcinogenesis over Time through Urine Proteome Profiling in an Animal Model: An Exploratory Approach.International journal of molecular sciences · 2022Article
- Multigene Profiling of Circulating Tumor Cells (CTCs) for Prognostic Assessment in Treatment-Naïve Metastatic Hormone-Sensitive Prostate Cancer (mHSPC).International journal of molecular sciences · 2021Article
- Paradoxical Roles of Desmosomal Components in Head and Neck Cancer.Biomolecules · 2021Review
- BST2 regulates interferon gamma-dependent decrease in invasion of HTR-8/SVneo cells via STAT1 and AKT signaling pathways and expression of E-cadherin.Cell adhesion & migration · 2020Article
- Significance of desmoglein-2 on cell malignant behaviors via mediating MAPK signaling in cervical cancer.The Kaohsiung journal of medical sciences · 2020Article
- LZAP promotes the proliferation and invasiveness of cervical carcinoma cells by targeting AKT and EMT.Journal of Cancer · 2020Article
- Thioredoxin Downregulation Enhances Sorafenib Effects in Hepatocarcinoma Cells.Antioxidants (Basel, Switzerland) · 2019Article
- Pard3 suppresses glioma invasion by regulating RhoA through atypical protein kinase C/NF-κB signaling.Cancer medicine · 2019Article
- Article
- Suppressing growth and invasion of human hepatocellular carcinoma cells by celecoxib through inhibition of cyclooxygenase-2.Cancer management and research · 2019Article
- Alterations of COX-2, HER-2/neu and E-Cadherin protein expression in the prostatic adenocarcinoma: preliminary findings.American journal of translational research · 2019Article
- Protein Phosphatase 2A: More Than a Passenger in the Regulation of Epithelial Cell-Cell Junctions.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Reduced expression of both classical and desmosomal cadherins has been associated with different types of carcinomas, including prostate cancer. This study aims to provide a comprehensive view of the role and regulation of cell-cell adhesion in prostate cancer aggressiveness by examining the functional implications of both E-cadherin and Desmoglein 2 (DSG2). E-cadherin expression was first examined using immunofluorescence in 50 normal prostate tissues and in a cohort of 414 prostate cancer patients. Correlation and survival analyses were performed to assess its clinical significance. In primary prostate cancer patients, reduced expression of both E-cadherin and DSG2 is significantly associated with an earlier biochemical recurrence. Transgenic DU145 E-cadherin knockdown and constitutively active AKT overexpression lines were generated. Functional implications of such genetic alterations were analyzed in vitro and in vivo, the latter by using tumorigenesis as well as extravasation and metastatic tumor formation assays. We observed that loss of E-cadherin leads to impaired primary and metastatic tumor formation in vivo, suggesting a tumor promoter role for E-cadherin in addition to its known role as a tumor suppressor. Activation of AKT leads to a significant reduction in E-cadherin expression and nuclear localization of Snail, suggesting a role for the PI3K/AKT signaling pathway in the transient repression of E-cadherin. This reduced expression may be regulated by separate mechanisms as neither the loss of E-cadherin nor activation of AKT significantly affected DSG2 expression. In conclusion, these findings illustrate the critical role of cell-cell adhesion in the progression to aggressive prostate cancer, through regulation by the PI3K pathway.
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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.