ArticleMolecular biology of the cell2005
TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition.
Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 316 papers, 1 of them a synthesis that pooled it.
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Who cites it
316 citing papers in PubMed, 1 synthesis or guideline pooled it, 587 citations in OpenAlex.
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- Assessing the therapeutic effects of DPP4 Inhibitors on TGF-β2-induced Lens Opacity.Experimental eye research · 2026Article
- Transcriptomic analysis of zonula occludens-1 (ZO-1) knockout in ovarian cancer cell lines.Genes & genomics · 2026Article
- Oxymatrine Inhibits Epithelial-Mesenchymal Transition to Alleviate Airway Remodeling in Chronic Obstructive Pulmonary Disease by Suppressing the TGF-β1/Smad Pathway.The Kaohsiung journal of medical sciences · 2026Article
- Deciphering the role of glycolipids as emerging therapeutic targets in EMT-driven cancer progression.Discover oncology · 2026Review
- Calcific aortic valve disease: can targeting endothelial-mesenchymal transition be a new alternative to surgery?-a narrative review.Cardiovascular diagnosis and therapy · 2026Review
- Predominant miRNAs in Animal-Source Foods and Bioinformatic Analysis.Current issues in molecular biology · 2026Article
- SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026Review
- Curcumin suppresses EMT to alleviate oral submucous fibrosis progression through XIST/miR-25-3p-mediated inactivation of the TGF-β1/Smads signalling pathway.International dental journal · 2026Article
- The long noncoding RNA VIM-AS1 and nucleoporin Nup358/RanBP2 regulate SMAD nuclear accumulation during TGF-β signaling.Nucleic acids research · 2026Article
- S100B drives glioblastoma invasion and migration through TGF‑β2‑mediated epithelial‑mesenchymal transition.Oncology reports · 2026Article
- Bee Venom and Cancer: A Mini-review Focusing on Melittin Antitumoral Effects.Current drug targets · 2026Review
- Disrupting the TGF-β-regulated epithelial-mesenchymal transition, apoptotic and autophagic phenotypes of 3D glioblastoma spheroids via glycolytic inhibition.Exploration of targeted anti-tumor therapy · 2026Article
- Distinct transcriptional regulation of the Wnt and TGFβ signaling families associated with wound healing and fibrotic outcomes to lens injury.Experimental eye research · 2025Article
- Feasibility IB trial of paclitaxel/carboplatin + Galunisertib. (a small molecule inhibitor of the kinase domain of type 1 TGF-B receptor) in patients with newly diagnosed, persistent or recurrent carcinosarcoma of the uterus or ovary.Gynecologic oncology · 2025Article
- Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells.Journal of advanced research · 2025Article
- Regulation of Renal Transporters by Pro-inflammatory Cytokines in Human Proximal Tubular Epithelial Cells: Identification of the Perpetrator and Mechanisms.bioRxiv : the preprint server for biology · 2025Article
256 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) contributes to normal tissue patterning and carcinoma invasiveness. We show that transforming growth factor (TGF)-beta/activin members, but not bone morphogenetic protein (BMP) members, can induce EMT in normal human and mouse epithelial cells. EMT correlates with the ability of these ligands to induce growth arrest. Ectopic expression of all type I receptors of the TGF-beta superfamily establishes that TGF-beta but not BMP pathways can elicit EMT. Ectopic Smad2 or Smad3 together with Smad4 enhanced, whereas dominant-negative forms of Smad2, Smad3, or Smad4, and wild-type inhibitory Smad7, blocked TGF-beta-induced EMT. Transcriptomic analysis of EMT kinetics identified novel TGF-beta target genes with ligand-specific responses. Using a TGF-beta type I receptor that cannot activate Smads nor induce EMT, we found that Smad signaling is critical for regulation of all tested gene targets during EMT. One such gene, Id2, whose expression is repressed by TGF-beta1 but induced by BMP-7 is critical for regulation of at least one important myoepithelial marker, alpha-smooth muscle actin, during EMT. Thus, based on ligand-specific responsiveness and evolutionary conservation of the gene expression patterns, we begin deciphering a genetic network downstream of TGF-beta and predict functional links to the control of cell proliferation and EMT.
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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.