ReviewJournal of mammary gland biology and neoplasia2010
Cell polarity in motion: redefining mammary tissue organization through EMT and cell polarity transitions.
Review in Journal of mammary gland biology and neoplasia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 77 citations in OpenAlex.
- Review
- Regulation of Cell Adhesion and Migration via Microtubule Cytoskeleton Organization, Cell Polarity, and Phosphoinositide Signaling.Biomolecules · 2023Review
- Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.The Japanese dental science review · 2022Review
- Colostrogenesis: Role and Mechanism of the Bovine Fc Receptor of the Neonate (FcRn).Journal of mammary gland biology and neoplasia · 2021Review
- Orchestration of tissue-scale mechanics and fate decisions by polarity signalling.The EMBO journal · 2021Review
- Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Identification and Verification of Two Novel Differentially Expressed Proteins from Non-neoplastic Mucosa and Colorectal Carcinoma Via iTRAQ Combined with Liquid Chromatography-Mass Spectrometry.Pathology oncology research : POR · 2020Article
- Immunoregulatory protein B7-H3 regulates cancer stem cell enrichment and drug resistance through MVP-mediated MEK activation.Oncogene · 2019Article
- Cellular plasticity and metastasis in breast cancer: a pre- and post-malignant problem.Journal of cancer metastasis and treatment · 2019Article
- No evidence of involvement of E-cadherin in cell fate specification or the segregation of Epi and PrE in mouse blastocysts.PloS one · 2019Article
- Claudins in morphogenesis: Forming an epithelial tube.Tissue barriers · 2017Review
- The Emerging Role of Polo-Like Kinase 1 in Epithelial-Mesenchymal Transition and Tumor Metastasis.Cancers · 2017Review
- VGLL4 Selectively Represses YAP-Dependent Gene Induction and Tumorigenic Phenotypes in Breast Cancer.Scientific reports · 2017Article
- TRIM37 promotes epithelial‑mesenchymal transition in colorectal cancer.Molecular medicine reports · 2017Article
- β-Catenin haploinsufficiency promotes mammary tumorigenesis in an ErbB2-positive basal breast cancer model.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Polarity Reversal by Centrosome Repositioning Primes Cell Scattering during Epithelial-to-Mesenchymal Transition.Developmental cell · 2017Article
- Intracellular Golgi Complex organization reveals tissue specific polarity during zebrafish embryogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2016Article
- Epithelial-mesenchymal transition during extravillous trophoblast differentiation.Cell adhesion & migration · 2016Article
- The ubiquitin ligase Smurf2 suppresses TGFβ-induced epithelial-mesenchymal transition in a sumoylation-regulated manner.Cell death and differentiation · 2016Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial to mesenchymal transition (EMT) and its reversion via mesenchymal to epithelial transition (MET), represent a stepwise cycle of epithelial plasticity that allows for normal tissue remodelling and diversification during development. In particular, epithelial-mesenchymal plasticity is central to many aspects of mammary development and has been proposed to be a key process in breast cancer progression. Such epithelial-mesenchymal plasticity requires complex cellular reprogramming to orchestrate a change in cell shape to an alternate morphology more conducive to migration. During this process, epithelial characteristics, including apical-basal polarity and specialised cell-cell junctions are lost and mesenchymal properties, such as a front-rear polarity associated with weak cell-cell contacts, increased motility, resistance to apoptosis and invasiveness are gained. The ability of epithelial cells to undergo transitions through cell polarity states is a central feature of epithelial-mesenchymal plasticity. These cell polarity states comprise a set of distinct asymmetric distributions of cellular constituents that are fashioned to allow specialized cellular functions, such as the regulated homeostasis of molecules across epithelial barriers, cell migration or cell diversification via asymmetric cell divisions. Each polarity state is engineered using a molecular toolbox that is highly conserved between organisms and cell types which can direct the initiation, establishment and continued maintenance of each asymmetry. Here we discuss how EMT pathways target cell polarity mediators, and how this EMT-dependent change in polarity states impact on the various stages of breast cancer. Emerging evidence places cell polarity at the interface of proliferation and morphology control and as such the changing dynamics within polarity networks play a critical role in normal mammary gland development and breast cancer progression.
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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.