ArticleCancer research2008
The polarity protein Par6 induces cell proliferation and is overexpressed in breast cancer.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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
86 citing papers in PubMed, 138 citations in OpenAlex.
- Integrative genetic analysis identifies shared regulation of DNA methylation and gene expression in migraine risk.The journal of headache and pain · 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
- Par6/SOX2 interact to modulate stemness maintenance in glioma by regulating the EGFR/PI3K/AKT signaling cascade.Oncogene · 2025Article
- Polarity Gene PARD6B Promotes Tumor Growth of Colorectal Cancer via Increasing MYC Expression.Cancer science · 2025Article
- Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis.The Journal of experimental medicine · 2025Article
- Review
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Spatial multiomic landscape of the human placenta at molecular resolution.Nature medicine · 2024Article
- PARD6A promotes lung adenocarcinoma cell proliferation and invasion through Serpina3.Cancer gene therapy · 2024Article
- Comprehensive proteomic analysis reveals omega-3 fatty acids to counteract endotoxin-stimulated metabolic dysregulation in porcine enterocytes.Scientific reports · 2023Article
- 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
- Cell polarity and cell adhesion associated gene expression differences between invasive micropapillary and no special type breast carcinomas and their prognostic significance.Scientific reports · 2021Article
- CD13 orients the apical-basal polarity axis necessary for lumen formation.Nature communications · 2021Article
- Molecular subversion of Cdc42 signalling in cancer.Biochemical Society transactions · 2021Review
- The molecular basis of mammary gland development and epithelial differentiation.Seminars in cell & developmental biology · 2021Review
- Article
- The Scribble family in cancer: twentieth anniversary.Oncogene · 2020Review
- High expression of DLG3 is associated with decreased survival from breast cancer.Clinical and experimental pharmacology & physiology · 2019Article
- Loss of cell polarity regulated by PTEN/Cdc42 enrolled in the process of Hepatopulmonary Syndrome.Journal of cellular and molecular medicine · 2019Article
26 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
The polarity protein complex Par6/atypical protein kinase (aPKC)/Cdc42 regulates polarization processes during epithelial morphogenesis, astrocyte migration, and axon specification. We, as well as others, have shown that this complex is also required for disruption of apical-basal polarity during the oncogene ErbB2-induced transformation and transforming growth factor beta-induced epithelial-mesenchymal transition of mammary epithelial cells. Here, we report that expression of Par6 by itself in mammary epithelial cells induces epidermal growth factor-independent cell proliferation and development of hyperplastic three-dimensional acini without affecting apical-basal polarity. This is dependent on the ability of Par6 to interact with aPKC and Cdc42, but not Lgl and Par3, and its ability to promote sustained activation of MEK/ERK signaling. Down-regulation of Cdc42 or aPKC expression suppresses the ability of Par6 to induce proliferation, demonstrating that Par6 promotes cell proliferation by interacting with aPKC and Cdc42. We also show that Par6 is overexpressed in breast cancer-derived cell lines and in both precancerous breast lesions and advanced primary human breast cancers, suggesting that Par6 overexpression regulates tumor initiation and progression. Thus, in addition to regulating cell polarization processes, Par6 is an inducer of cell proliferation in breast epithelial cells.
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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.