Related Experiment Video
Updated: Mar 17, 2026

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
Chemical regulators of epithelial plasticity reveal a nuclear receptor pathway controlling myofibroblast
Jon M Carthy1, Martin Stöter2, Claudia Bellomo1,3
1Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Box 595, Biomedical Center, SE-751 24 Uppsala, Sweden.
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.
Related Concept Videos
Master Transcription Regulators
TGF - β Signaling Pathway
Methods of Nuclear Reprogramming
Transducer Mechanism: Nuclear Receptors
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
Somatic to iPS Cell Reprogramming
Introduction to Fibroblasts

