ArticleScientific reports2016
Chemical regulators of epithelial plasticity reveal a nuclear receptor pathway controlling myofibroblast differentiation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Liver X Receptors Enhance Epithelial to Mesenchymal Transition in Metastatic Prostate Cancer Cells.Cancers · 2024Article
- Liver X receptor alpha ensures blood-brain barrier function by suppressing SNAI2.Cell death & disease · 2023Article
- LXRα limits TGFβ-dependent hepatocellular carcinoma associated fibroblast differentiation.Oncogenesis · 2019Article
- Primary cell-based phenotypic assays to pharmacologically and genetically study fibrotic diseasesJournal of biological methods · 2019Article
- Snail mediates crosstalk between TGFβ and LXRα in hepatocellular carcinoma.Cell death and differentiation · 2018Article
- Dual function of TGFβ in lens epithelial cell fate: implications for secondary cataract.Molecular biology of the cell · 2017Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasticity in epithelial tissues relates to processes of embryonic development, tissue fibrosis and cancer progression. Pharmacological modulation of epithelial transitions during disease progression may thus be clinically useful. Using human keratinocytes and a robotic high-content imaging platform, we screened for chemical compounds that reverse transforming growth factor β (TGF-β)-induced epithelial-mesenchymal transition. In addition to TGF-β receptor kinase inhibitors, we identified small molecule epithelial plasticity modulators including a naturally occurring hydroxysterol agonist of the liver X receptors (LXRs), members of the nuclear receptor transcription factor family. Endogenous and synthetic LXR agonists tested in diverse cell models blocked α-smooth muscle actin expression, myofibroblast differentiation and function. Agonist-dependent LXR activity or LXR overexpression in the absence of ligand counteracted TGF-β-mediated myofibroblast terminal differentiation and collagen contraction. The protective effect of LXR agonists against TGF-β-induced pro-fibrotic activity raises the possibility that anti-lipidogenic therapy may be relevant in fibrotic disorders and advanced cancer.
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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.