ArticleDevelopmental cell2014
Mammary morphogenesis and regeneration require the inhibition of EMT at terminal end buds by Ovol2 transcriptional repressor.
Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 197 citations in OpenAlex.
- OVOL2 reinforces epithelial identity and promotes SynT-I differentiation in the mouse placenta†.Biology of reproduction · 2026Article
- Mesenchymal to epithelial transition (MET) in cancer progression: insights from logical modeling.Scientific reports · 2026Article
- Transcriptional coordination in multicellular lineage differentiation during lung organogenesis: deciphering the role of epithelial cells as a microenvironmental regulatory hub.Frontiers in cell and developmental biology · 2026Review
- Stemness regulation in prostate cancer: prostate cancer stem cells and targeted therapy.Annals of medicine · 2025Review
- Targeted therapy for liver cancer: Current status and future directions.BioImpacts : BI · 2025Review
- Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025Review
- Differential chromatin accessibility and transcriptional dynamics define breast cancer subtypes and their lineages.Nature cancer · 2024Article
- Disruption of perinatal myeloid niches impacts the aging clock of pancreatic β cells.iScience · 2024Article
- Phenotypic Plasticity and Cancer: A System Biology Perspective.Journal of clinical medicine · 2024Review
- Cancer cell plasticity: from cellular, molecular, and genetic mechanisms to tumor heterogeneity and drug resistance.Cancer metastasis reviews · 2024Review
- Crosstalk between chromatin and Shavenbaby defines transcriptional output along the Drosophila intestinal stem cell lineage.iScience · 2024Article
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- Single-cell Analysis Reveals Inter- and Intratumour Heterogeneity in Metastatic Breast Cancer.Journal of mammary gland biology and neoplasia · 2023Article
- OVOL2 sustains postnatal thymic epithelial cell identity.Nature communications · 2023Article
- Single-cell and spatial analyses reveal a tradeoff between murine mammary proliferation and lineage programs associated with endocrine cues.Cell reports · 2023Article
- OVOL2: an epithelial lineage determiner with emerging roles in energy homeostasis.Trends in cell biology · 2023Review
- Epithelial-Mesenchymal Plasticity and Endothelial-Mesenchymal Transition in Cutaneous Wound Healing.Cold Spring Harbor perspectives in biology · 2023Review
- ZHX2 deficiency enriches hybrid MET cells through regulating E-cadherin expression.Cell death & disease · 2023Article
- Ovol1/2 loss-induced epidermal defects elicit skin immune activation and alter global metabolism.EMBO reports · 2023Article
- Heterogeneity and plasticity of epithelial-mesenchymal transition (EMT) in cancer metastasis: Focusing on partial EMT and regulatory mechanisms.Cell proliferation · 2023Review
63 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial cells possess remarkable plasticity, having the ability to become mesenchymal cells through alterations in adhesion and motility (epithelial-to-mesenchymal transition [EMT]). However, how epithelial plasticity is kept in check in epithelial cells during tissue development and regeneration remains to be fully understood. Here we show that restricting the EMT of mammary epithelial cells by transcription factor Ovol2 is required for proper morphogenesis and regeneration. Deletion of Ovol2 blocks mammary ductal morphogenesis, depletes stem and progenitor cell reservoirs, and leads epithelial cells to undergo EMT in vivo to become nonepithelial cell types. Ovol2 directly represses myriad EMT inducers, and its absence switches response to TGF-β from growth arrest to EMT. Furthermore, forced expression of the repressor isoform of Ovol2 is able to reprogram metastatic breast cancer cells from a mesenchymal to an epithelial state. Our findings underscore the critical importance of exquisitely regulating epithelial plasticity in development and cancer.
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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.