ArticleProceedings of the National Academy of Sciences of the United States of America2017
EMT programs promote basal mammary stem cell and tumor-initiating cell stemness by inducing primary ciliogenesis and Hedgehog signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 150 citations in OpenAlex.
- Primary cilia connect epithelial mesenchymal plasticity with anoikis resistance and cancer stemness.Discover oncology · 2026Review
- Co-mutations of CTNNB1 and PTEN drive aggressive tumor progression in endometrial cancer.Disease models & mechanisms · 2026Article
- Primary ciliogenesis is promoted during epithelial-mesenchymal transition via a miR-200 - DZIP1 axis.Cell communication and signaling : CCS · 2026Article
- Article
- 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
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Article
- Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment.International journal of molecular sciences · 2024Review
- CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.Cell death & disease · 2024Article
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- The implication of ciliary signaling pathways for epithelial-mesenchymal transition.Molecular and cellular biochemistry · 2024Review
- A tumor suppressor protein encoded by circKEAP1 inhibits osteosarcoma cell stemness and metastasis by promoting vimentin proteasome degradation and activating anti-tumor immunity.Journal of experimental & clinical cancer research : CR · 2024Article
- Mechanosensitive hormone signaling promotes mammary progenitor expansion and breast cancer risk.Cell stem cell · 2024Article
- Primary cilia-associated signalling in squamous cell carcinoma of head and neck region.Frontiers in oncology · 2024Review
- The relationship between HYDIN and fallopian tubal cilia loss in patients with epithelial ovarian cancer.Frontiers in oncology · 2024Article
- Single-cell transcriptomic analysis uncovers the origin and intratumoral heterogeneity of parotid pleomorphic adenoma.International journal of oral science · 2023Article
- Matrix obstructions cause multiscale disruption in collective epithelial migration by suppressing leader cell function.Molecular biology of the cell · 2023Article
- Extracellular Vesicles in Breast Cancer: From Biology and Function to Clinical Diagnosis and Therapeutic Management.International journal of molecular sciences · 2023Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue regeneration relies on adult stem cells (SCs) that possess the ability to self-renew and produce differentiating progeny. In an analogous manner, the development of certain carcinomas depends on a small subset of tumor cells, called "tumor-initiating cells" (TICs), with SC-like properties. Mammary SCs (MaSCs) reside in the basal compartment of the mammary epithelium, and their neoplastic counterparts, mammary TICs (MaTICs), are thought to serve as the TICs for the claudin-low subtype of breast cancer. MaSCs and MaTICs both use epithelial-mesenchymal transition (EMT) programs to acquire SC properties, but the mechanism(s) connecting EMT programs to stemness remain unclear. Here we show that this depends on primary cilia, which are nonmotile, cell-surface structures that serve as platforms for receiving cues and enable activation of various signaling pathways. We show that MaSC and MaTIC EMT programs induce primary cilia formation and Hedgehog (Hh) signaling, which has previously been implicated in both MaSC and MaTIC function. Moreover, ablation of these primary cilia is sufficient to repress Hh signaling, the stemness of MaSCs, and the tumor-forming potential of MaTICs. Together, our findings establish primary ciliogenesis and consequent Hh signaling as a key mechanism by which MaSC and MaTIC EMT programs promote stemness and thereby support mammary tissue outgrowth and tumors of basal origin.
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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.