ArticleCellular signalling2017
Downregulation of PKCζ/Pard3/Pard6b is responsible for lung adenocarcinoma cell EMT and invasion.
Article in Cellular signalling, 2017. 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, 43 citations in OpenAlex.
- Drugging non-canonical kinases in cancer therapeutics: Molecular targets, underlying mechanisms and small-molecule inhibitors.Acta pharmaceutica Sinica. B · 2026Review
- HyPIC-3D enables characterization of migratory cancer cell subpopulations in 3D hypoxic microenvironments.Cell reports methods · 2026Article
- Apicobasal Polarity Protein PARD3 Plays an Essential Role in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2026Article
- Polarity Gene PARD6B Promotes Tumor Growth of Colorectal Cancer via Increasing MYC Expression.Cancer science · 2025Article
- Protein kinase C zeta promotes thyroid Cancer progression and represents a novel therapeutic target: evidence from specific atypical PKC inhibitor 2-acetyl-1,3-cyclopentanedione inhibitor studies.Frontiers in medicine · 2025Article
- Perturbation of mammary epithelial cell apicobasal polarity by RHBDF1-facilitated nuclear translocation of PKCζ.Biological research · 2024Article
- PARD3 drives tumorigenesis through activating Sonic Hedgehog signalling in tumour-initiating cells in liver cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Microvascular smooth muscle cells exhibit divergent phenotypic switching responses to platelet-derived growth factor and insulin-like growth factor 1.Microvascular research · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3.Cancer cell international · 2023Article
- Snapshot imprinting as a tool for surface mapping and identification of novel biomarkers of senescent cells.Nanoscale advances · 2022Article
- Separable mechanisms drive local and global polarity establishment in the Caenorhabditiselegans intestinal epithelium.Development (Cambridge, England) · 2022Article
- Induced retinal pigment epithelial cells with anti-epithelial-to-mesenchymal transition ability delay retinal degeneration.iScience · 2022Article
- Article
- Partitioning defective 6 homolog alpha (PARD6A) promotes epithelial-mesenchymal transition via integrin β1-ILK-SNAIL1 pathway in ovarian cancer.Cell death & disease · 2022Article
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- Sex Comb on Midleg Like-2 Accelerates Hepatocellular Carcinoma Cell Proliferation and Metastasis by Activating Wnt/β-Catenin/EMT Signaling.Yonsei medical journal · 2021Article
- The polarity protein PARD3 and cancer.Oncogene · 2021Review
- High expression of PARD3 predicts poor prognosis in hepatocellular carcinoma.Scientific reports · 2021Article
- Selection of microRNAs in extracellular vesicles for diagnosis of malignant pleural mesothelioma by in vitro analysis.Oncology reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Atypical protein kinase C ζ (PKCζ) forms an apico-basal polarity complex with Partitioning Defective (Pard) 3 and Pard6 to regulate normal epithelial cell apico-basolateral polarization. The dissociation of the PKCζ/Pard3/Pard6 complex is essential for the disassembly of the tight/adherens junction and epithelial-mesenchymal transition (EMT) that is critical for tumor spreading. Loss of cell polarity and epithelial organization is strongly correlated with malignancy and tumor progression in some other cancer types. However, it is unclear whether the PKCζ/Pard3/Pard6 complex plays a role in the progression of non-small-cell lung cancer (NSCLC). We found that hypoxia downregulated the PKCζ/Pard3/Pard6 complex, correlating with induction of lung cancer cell migration and invasion. Silencing of the PKCζ/Pard3/Pard6 polarity complex components induced lung cancer cell EMT, invasion, and colonization in vivo. Suppression of Pard3 was associated with altered expression of genes regulating wound healing, cell apoptosis/death and cell motility, and particularly upregulation of MAP3K1 and fibronectin which are known to contribute to lung cancer progression. Human lung adenocarcinoma tissues expressed less Pard6b and PKCζ than the adjacent normal tissues and in experimental mouse lung adenocarcinoma, the levels of Pard3 and PKCζ were also decreased. In addition, we showed that a methylation locus in the gene body of Pard3 is positively associated with the expression of Pard3 and that methylation of the Pard3 gene increased cellular sensitivity to carboplatin, a common chemotherapy drug. Suppression of Pard3 increased chemoresistance in lung cancer cells. Together, these results suggest that reduced expression of PKCζ/Pard3/Pard6 contributes to NSCLC EMT, invasion, and chemoresistance.
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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.