ArticleScience advances2021
An EMT-primary cilium-GLIS2 signaling axis regulates mammogenesis and claudin-low breast tumorigenesis.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Primary cilium as a sensory organelle and metabolic hub in health and diseases.Journal of biomedical science · 2026Review
- Primary cilia connect epithelial mesenchymal plasticity with anoikis resistance and cancer stemness.Discover oncology · 2026Review
- Pathophysiological significance of cholesterol in ciliopathies.Fujita medical journal · 2026Article
- Primary ciliogenesis is promoted during epithelial-mesenchymal transition via a miR-200 - DZIP1 axis.Cell communication and signaling : CCS · 2026Article
- Interplay between Epigenetic and Transcription Factors Mediating Drug Resistance via Stem Cells in Breast Cancer.ACS omega · 2025Review
- Taking Down the Primary Cilium: Pathways for Disassembly in Differentiating Cells.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- EMT-ciliary signaling in quasi-mesenchymal-stem-like cells drives therapeutic resistance and is a druggable vulnerability in triple-negative breast cancer.EMBO molecular medicine · 2025Article
- A type of pancreatic cancer cells form cell clusters from a solitary condition in a primary ciliogenesis-dependent manner.Medical molecular morphology · 2025Article
- Primary cilia and cancer: a tale of many faces.Oncogene · 2025Review
- The proximity-based protein interactome and regulatory logics of the transcription factor p65 NF-κB/RELA.EMBO reports · 2025Article
- Article
- CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.Cell death & disease · 2024Article
- The implication of ciliary signaling pathways for epithelial-mesenchymal transition.Molecular and cellular biochemistry · 2024Review
- Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease.Nature communications · 2024Article
- The relationship between HYDIN and fallopian tubal cilia loss in patients with epithelial ovarian cancer.Frontiers in oncology · 2024Article
- Primary cilia-associated signalling in squamous cell carcinoma of head and neck region.Frontiers in oncology · 2024Review
- Cholesterol in the ciliary membrane as a therapeutic target against cancer.Frontiers in molecular biosciences · 2023Review
- Epithelial-mesenchymal transition in cancer stemness and heterogeneity: updated.Medical oncology (Northwood, London, England) · 2022Review
- Review
- Anhydroicaritin Inhibits EMT in Breast Cancer by Enhancing GPX1 Expression: A Research Based on Sequencing Technologies and Bioinformatics Analysis.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
22 authors at 10 institutions in 3 countries.
Funding
Abstract
The epithelial-mesenchymal transition (EMT) and primary ciliogenesis induce stem cell properties in basal mammary stem cells (MaSCs) to promote mammogenesis, but the underlying mechanisms remain incompletely understood. Here, we show that EMT transcription factors promote ciliogenesis upon entry into intermediate EMT states by activating ciliogenesis inducers, including FGFR1. The resulting primary cilia promote ubiquitination and inactivation of a transcriptional repressor, GLIS2, which localizes to the ciliary base. We show that GLIS2 inactivation promotes MaSC stemness, and GLIS2 is required for normal mammary gland development. Moreover, GLIS2 inactivation is required to induce the proliferative and tumorigenic capacities of the mammary tumor–initiating cells (MaTICs) of claudin-low breast cancers. Claudin-low breast tumors can be segregated from other breast tumor subtypes based on a GLIS2-dependent gene expression signature. Collectively, our findings establish molecular mechanisms by which EMT programs induce ciliogenesis to control MaSC and MaTIC stemness, mammary gland development, and claudin-low breast cancer formation.
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.