ArticleNature cell biology2013
Loss of Par3 promotes breast cancer metastasis by compromising cell-cell cohesion.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
107 citing papers in PubMed, 158 citations in OpenAlex.
- Glycolytic suppression of cell adhesion promotes thyroid morphogenesis in response to nutrition.EMBO reports · 2026Article
- Apicobasal Polarity Protein PARD3 Plays an Essential Role in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2026Article
- The polarity protein Par3 enhances renal cell carcinoma metastasisCancer biology & medicine · 2025Article
- Pard3 promotes corneal epithelial stratification and homeostasis by regulating apical-basal polarity, cytoskeletal organization and tight junction-mediated barrier function.The ocular surface · 2025Article
- Review
- Ferroptosis - a potential feature underlying neratinib-induced colonic epithelial injury.Cancer chemotherapy and pharmacology · 2024Article
- Cell polarity changes in cancer initiation and progression.The Journal of cell biology · 2024Review
- TMEM25 is a Par3-binding protein that attenuates claudin assembly during tight junction development.EMBO reports · 2024Article
- Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3.Cancer cell international · 2023Article
- Cytokeratins 5 and 17 Maintain an Aggressive Epithelial State in Basal-Like Breast Cancer.Molecular cancer research : MCR · 2022Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages.Nature communications · 2022Review
- LGL1 binds to Integrin β1 and inhibits downstream signaling to promote epithelial branching in the mammary gland.Cell reports · 2022Article
- Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest.Breast cancer research and treatment · 2022Article
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- Hyaluronan synthase 2 (HAS2) regulates cell phenotype and invadopodia formation in luminal-like breast cancer cells.Molecular and cellular biochemistry · 2021Article
- Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis.Cancer science · 2021Article
- Orchestration of tissue-scale mechanics and fate decisions by polarity signalling.The EMBO journal · 2021Review
- The molecular basis of mammary gland development and epithelial differentiation.Seminars in cell & developmental biology · 2021Review
- The polarity protein PARD3 and cancer.Oncogene · 2021Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The mechanisms by which tumour cells metastasize and the role that cell polarity proteins play in this process are not well understood. We report that partitioning defective protein 3 (Par3) is dysregulated in metastasis in human breast cancer, and is associated with a higher tumour grade and ErbB2-positive status. Downregulation of Par3 cooperated with ErbB2 to induce cell invasion and metastasis in vivo. Interestingly, the metastatic behaviour was not associated with an overt mesenchymal phenotype. However, loss of Par3 inhibited E-cadherin junction stability, disrupted membrane and actin dynamics at cell-cell junctions and decreased cell-cell cohesion in a manner dependent on the Tiam1/Rac-GTP pathway. Inhibition of this pathway restored E-cadherin junction stability and blocked invasive behaviour of cells lacking Par3, suggesting that loss of Par3 promotes metastatic behaviour of ErbB2-induced tumour epithelial cells by decreasing cell-cell cohesion.
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Identifiers
What 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.