ArticleNature communications2022
Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- The Regulation and Function of Hippo/YAP Pathway in Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- LATS1/2 Inhibitor Attenuates Osteoclast Differentiation via Hippo-YAP/TAZ Signaling Pathway and Alleviates Osteoporosis in Ovariectomized Rats.Current medical science · 2026Article
- Lats1/2 Differentially Modulate the Proliferative State of Dental Epithelial Progenitors and Ameloblasts in the Murine Incisor.Orthodontics & craniofacial research · 2025Article
- 3D printing-biomimetic local stiff niche enhances glycolysis to boost PDAC cell stem-like phenotype via N6-methyladenosine-suppressed YAP1 mRNA decay.Materials today. Bio · 2025Article
- TEAD-targeting small molecules induce a cofactor switch to regulate the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Intraductal Injection of Adenoviruses to Perform Lineage Tracing in the Mammary Gland.Journal of mammary gland biology and neoplasia · 2025Review
- A novel clinically relevant antagonistic interplay between prolactin and oncogenic YAP-CCN2 pathways as a differentiation therapeutic target in breast cancer.Cell death & disease · 2025Article
- Noncanonical Wnt/Ror2 Signaling Regulates Basal Cell Fidelity and Branching Morphogenesis in the Mammary Gland.bioRxiv : the preprint server for biology · 2025Article
- Role and therapeutic potential of the NEDD4 family in breast cancer.Frontiers in pharmacology · 2025Review
- METTL14 suppresses the expression of YAP1 and the stemness of triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Increased prevalence of hybrid epithelial/mesenchymal state and enhanced phenotypic heterogeneity in basal breast cancer.iScience · 2024Article
- TRPS1 maintains luminal progenitors in the mammary gland by repressing SRF/MRTF activity.Breast cancer research : BCR · 2024Article
- CCDC25 suppresses clear cell renal cell carcinoma progression by LATS1/YAP-mediated regulation of the hippo pathway.Cancer cell international · 2024Article
- ID4-dependent secretion of VEGFA enhances the invasion capability of breast cancer cells and activates YAP/TAZ via integrin β3-VEGFR2 interaction.Cell death & disease · 2024Article
- Control of stem cell renewal and fate by YAP and TAZ.Nature reviews. Molecular cell biology · 2023Review
- New Insights into YAP/TAZ-TEAD-Mediated Gene Regulation and Biological Processes in Cancer.Cancers · 2023Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Basal-like breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of Krt14 and Sox9-expressing basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Gene expression analyses of LATS1/2-deleted mammary epithelial cells notably revealed a transcriptional program that associates with human basal-like breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal-like breast 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.