ArticleNature2017
The Hippo kinases LATS1 and 2 control human breast cell fate via crosstalk with ERα.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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The trial behind it
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Who cites it
95 citing papers in PubMed, 151 citations in OpenAlex.
- Blood-based detection of lung cancer using cysteine-rich angiogenic inducer 61 (CYR61) as a circulating protein biomarker: a pilot study.Molecular oncology · 2021Trial
- Impact of aromatase inhibitor treatment on global gene expression and its association with antiproliferative response in ER+ breast cancer in postmenopausal patients.Breast cancer research : BCR · 2019Trial
- SAV1 in Cooperation With FKBP52 Participates in Implantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ISGylation-mediated stabilization of CYP4Z1 fuels breast cancer initiation and progression.Experimental & molecular medicine · 2026Article
- Estrogen promotes osteogenesis via YAP1-driven activation of ERα orchestrated through TEAD1 binding to the ERα promoter.Journal of molecular histology · 2026Article
- The Regulation and Function of Hippo/YAP Pathway in Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- YAP1 Dysfunction Promotes Molecular Properties Linked to Breast Cancer Susceptibility.Cancer prevention research (Philadelphia, Pa.) · 2026Article
- Fluvastatin suppresses breast cancer initiation and progression via targeting CYP4Z1.Communications biology · 2026Article
- The Urinary Proteome Differs with the Presence and Type of Breast Cancer.Journal of proteome research · 2025Article
- Crosstalk between YAP/TAZ and ERα in mechanical and hormonal signaling in the skeletal system.Acta biochimica et biophysica Sinica · 2025Review
- Hippo signaling pathway in human testis and seminoma: anticancer effect of verteporfin on human seminoma TCam-2 cells.Journal of molecular histology · 2025Article
- Review
- HDAC inhibitors modulate Hippo pathway signaling in hormone positive breast cancer.Clinical epigenetics · 2025Article
- Targeting breast cancer stem cells in ER-positive breast cancer by repurposing the benzoporphyrin derivative verteporfin as a YAP/TAZ small molecule inhibitor.Molecular biology reports · 2025Article
- Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025Review
- Atypical Hippo signaling network: uncovering novel insights into head and neck cancer biology and advancements in precision intervention.Frontiers in cell and developmental biology · 2025Review
- Oncogene activated human breast luminal progenitors contribute basally located myoepithelial cells.Breast cancer research : BCR · 2024Article
- Single-cell EpiChem jointly measures drug-chromatin binding and multimodal epigenome.Nature methods · 2024Article
- LATS1 controls CTCF chromatin occupancy and hormonal response of 3D-grown breast cancer cells.The EMBO journal · 2024Article
- Hippo-YAP/TAZ signaling in breast cancer: Reciprocal regulation of microRNAs and implications in precision medicine.Genes & diseases · 2024Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 3 countries.
Funding
Abstract
Cell fate perturbations underlie many human diseases, including breast cancer. Unfortunately, the mechanisms by which breast cell fate are regulated are largely unknown. The mammary gland epithelium consists of differentiated luminal epithelial and basal myoepithelial cells, as well as undifferentiated stem cells and more restricted progenitors. Breast cancer originates from this epithelium, but the molecular mechanisms that underlie breast epithelial hierarchy remain ill-defined. Here, we use a high-content confocal image-based short hairpin RNA screen to identify tumour suppressors that regulate breast cell fate in primary human breast epithelial cells. We show that ablation of the large tumour suppressor kinases (LATS) 1 and 2 (refs 5, 6), which are part of the Hippo pathway, promotes the luminal phenotype and increases the number of bipotent and luminal progenitors, the proposed cells-of-origin of most human breast cancers. Mechanistically, we have identified a direct interaction between Hippo and oestrogen receptor-α (ERα) signalling. In the presence of LATS, ERα was targeted for ubiquitination and Ddb1-cullin4-associated-factor 1 (DCAF1)-dependent proteasomal degradation. Absence of LATS stabilized ERα and the Hippo effectors YAP and TAZ (hereafter YAP/TAZ), which together control breast cell fate through intrinsic and paracrine mechanisms. Our findings reveal a non-canonical (that is, YAP/TAZ-independent) effect of LATS in the regulation of human breast cell fate.
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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.