ArticleAmerican journal of cancer research2012
PAR6B is required for tight junction formation and activated PKCζ localization in breast cancer.
Article in American journal of cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 34 citations in OpenAlex.
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- Integrative multi-omics analysis identifies C-type lectin CNVs as functional targets for breeding mastitis-resistant dairy goats.Animal microbiome · 2026Article
- Differential expression of the lncRNA MIR17HG and miR-18a/miR-20a as candidate ncRNA signatures in stage II/III breast cancer and bioinformatic analysis of ncRNA-mRNA regulatory axes.Iranian journal of basic medical sciences · 2026Article
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- Case report: Complete paternal isodisomy on chromosome 18 induces methylation changes inFrontiers in genetics · 2023Article
- MicroRNA Profile of MA-104 Cell Line Associated With the Pathogenesis of Bovine Rotavirus Strain Circulated in Chinese Calves.Frontiers in microbiology · 2022Article
- Transcriptomic Analysis Reveals a Link Between Hippo Signaling Pathway and Macrophages in Lungs of Mice with OVA-Induced Allergic Asthma.Journal of inflammation research · 2022Article
- Identifying Novel Susceptibility Genes for Colorectal Cancer Risk From a Transcriptome-Wide Association Study of 125,478 Subjects.Gastroenterology · 2021Article
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- Dissecting the Effect of a 3D Microscaffold on the Transcriptome of Neural Stem Cells with Computational Approaches: A Focus on Mechanotransduction.International journal of molecular sciences · 2020Article
- Secreted breast tumor interstitial fluid microRNAs and their target genes are associated with triple-negative breast cancer, tumor grade, and immune infiltration.Breast cancer research : BCR · 2020Article
- Review
- Histone demethylase KDM3A is required for enhancer activation of hippo target genes in colorectal cancer.Nucleic acids research · 2019Article
- miR-130a and miR-212 Disrupt the Intestinal Epithelial Barrier through Modulation of PPARγ and Occludin Expression in Chronic Simian Immunodeficiency Virus-Infected Rhesus Macaques.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Decreased Expression of the Polarity Regulatory PAR Complex Predicts Poor Prognosis of the Patients with Colorectal Adenocarcinoma.Translational oncology · 2018Article
- Satellite Cells in Muscular Dystrophy - Lost in Polarity.Trends in molecular medicine · 2016Review
- Par6G suppresses cell proliferation and is targeted by loss-of-function mutations in multiple cancers.Oncogene · 2016Article
- ODAM is a predictor for biomedical recurrence and inhibits the migration and invasion of prostate cancer.American journal of translational research · 2016Article
- PKCζ Promotes Breast Cancer Invasion by Regulating Expression of E-cadherin and Zonula Occludens-1 (ZO-1) via NFκB-p65.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of mechanisms that govern the control of epithelial cell polarity, morphology and plasticity are emerging as key processes in tumor progression. In this study we report amplification and overexpression of PAR6B, an essential component in epithelial cell tight junction (TJ) formation and maintenance of apico-basal polarity, in breast cancer cell lines. Analysis of chromosome 20q13.13 in 11 breast cancer cell lines by fluorescence in situ hybridization (FISH) identified a novel small amplicon centered at PARD6B in 5 cell lines, with copy number ranging from 7 to 27. The presence of the PARD6B amplicon correlated with PARD6B transcript and PAR6B protein abundance. Expression of related isoforms PARD6A and PARD6G were detectable at significantly lower levels. PARD6B overexpression correlated with TJ network formation in cultured cell monolayers. SiRNA-mediated inhibition of PAR6B in MCF7 resulted in loss of TJ assembly and membrane localization of atypical PKCζ (aPKC), but did not affect adherens junction formation. SiRNA-mediated inhibition of CDC42 in MCF7 also resulted in loss of TJ networks, confirming the requirement of a complete PAR6-aPKC-CDC42-PAR3 complex to activate and stabilize TJs. Immunohistochemical analysis of PAR6B expression on breast tumor microarrays indicated exquisite epithelial cell-specificity. Few quantitative differences in staining were observed between normal epithelium and adjacent tumor margins. However staining appeared reduced and cytoplasmic in more poorly differentiated tumors. We propose that quantitative imbalances in the components of pathways governing normal epithelial cell polarity arising from gain or loss of function may radically alter epithelial cell architecture and contribute to tumor progression.
Indexed as
Identifiers
22957302PMC3433109W123467074What OpenQuestion holds
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.