Aristidis Moustakas

ORCID: 0000-0001-9131-3827
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About
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Research Areas
  • TGF-β signaling in diseases
  • Cancer Cells and Metastasis
  • Pancreatic and Hepatic Oncology Research
  • Cancer-related gene regulation
  • Genetic factors in colorectal cancer
  • Hedgehog Signaling Pathway Studies
  • Cell Adhesion Molecules Research
  • Kruppel-like factors research
  • Cancer-related molecular mechanisms research
  • Renal and related cancers
  • Cancer-related Molecular Pathways
  • RNA modifications and cancer
  • Hippo pathway signaling and YAP/TAZ
  • Metabolism, Diabetes, and Cancer
  • Epigenetics and DNA Methylation
  • Proteoglycans and glycosaminoglycans research
  • PARP inhibition in cancer therapy
  • Bone Metabolism and Diseases
  • Wnt/β-catenin signaling in development and cancer
  • RNA Research and Splicing
  • Ubiquitin and proteasome pathways
  • Fibroblast Growth Factor Research
  • Cancer, Hypoxia, and Metabolism
  • Liver physiology and pathology
  • Axon Guidance and Neuronal Signaling

Science for Life Laboratory
2016-2025

Uppsala University
2016-2025

Ludwig Cancer Research
2011-2021

Ludwig Cancer Research
2005-2015

Leiden University Medical Center
2013

Karolinska Institutet
2013

University of Crete
1998-2002

Foundation for Research and Technology Hellas
1998-2002

Humboldt State University
2002

Charité - Universitätsmedizin Berlin
2002

Abstract Long noncoding RNAs (lncRNAs) regulate gene expression by association with chromatin, but how they target chromatin remains poorly understood. We have used RNA immunoprecipitation-coupled high-throughput sequencing to identify 276 lncRNAs enriched in repressive from breast cancer cells. Using one of the chromatin-interacting lncRNAs, MEG3 , we explore mechanisms which chromatin. Here show that and EZH2 share common genes, including TGF-β pathway genes. Genome-wide mapping binding...

10.1038/ncomms8743 article EN cc-by Nature Communications 2015-07-24

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) can induce EMT in human mouse epithelial cells. correlates with the ability of these ligands arrest. Ectopic expression all type I receptors TGF-beta superfamily establishes BMP pathways elicit EMT. Smad2 or Smad3 together Smad4 enhanced, whereas dominant-negative forms Smad2,...

10.1091/mbc.e04-08-0658 article EN Molecular Biology of the Cell 2005-02-03

Epithelial–mesenchymal transition (EMT) occurs during embryogenesis, carcinoma invasiveness, and metastasis can be elicited by transforming growth factor-β (TGF-β) signaling via intracellular Smad transducers. The molecular mechanisms that control the onset of EMT remain largely unexplored. Transcriptomic analysis revealed high mobility group A2 (HMGA2) gene is induced pathway EMT. Endogenous HMGA2 mediates TGF-β, whereas ectopic causes irreversible characterized severe E-cadherin...

10.1083/jcb.200512110 article EN The Journal of Cell Biology 2006-07-10

The capacities of different transforming growth factor-(beta) (TGF-(beta)) superfamily members to drive epithelial mesenchymal transdifferentiation the murine mammary cell line NMuMG were investigated. TGF-(beta)1, but not activin A or osteogenic protein-1 (OP-1)/bone morphogenetic protein-7 (BMP-7), was able induce morphological transformation cells as shown by reorganisation actin cytoskeleton and relocalisation/downregulation E-cadherin (beta)-catenin, an effect that abrogated more...

10.1242/jcs.112.24.4557 article EN Journal of Cell Science 1999-12-15

Epithelial-mesenchymal transition (EMT) is important during embryonic cell layer movement and tumor invasiveness. EMT converts adherent epithelial cells to motile mesenchymal cells, favoring metastasis in the context of cancer progression. Transforming growth factor-beta (TGF-beta) triggers via intracellular Smad transducers other signaling proteins. We previously reported that high mobility group A2 (HMGA2) gene required for TGF-beta elicit mammary cells. In present study we investigated...

10.1074/jbc.m802016200 article EN cc-by Journal of Biological Chemistry 2008-10-03

Abstract Background Cancer cells are avid extracellular vesicle (EV) producers. EVs transport transforming growth factor-β (TGF-β), which is commonly activated under late stages of cancer progression. Nevertheless, whether TGF-β signaling coordinates EV biogenesis a relevant topic that remains minimally explored. Method We sought after specific pathway mediators could regulate release. To this end, we used large number cell models, coupled to biological assays, unbiased proteomic and...

10.1186/s13046-025-03291-0 article EN cc-by Journal of Experimental & Clinical Cancer Research 2025-02-06

The cell cycle inhibitor p21/WAF1/Cip1 is expressed in many types and regulated by p53-dependent p53-independent mechanisms. p21 an important regulator of hepatocyte cycle, differentiation, liver development, but little known about the regulation its synthesis hepatocytes. We report herein that gene constitutively human hepatoma HepG2 cells. Deletion analysis promoter showed it contains a distal (positions -2,300/-210) proximal -124 to -61) region act synergistically achieve high levels...

10.1073/pnas.95.12.6733 article EN Proceedings of the National Academy of Sciences 1998-06-09

Transforming growth factors beta (TGF-betas) inhibit of epithelial cells and induce differentiation changes, such as epithelial-mesenchymal transition (EMT). On the other hand, bone morphogenetic proteins (BMPs) weakly affect cell do not EMT. Smad4 transmits signals from both TGF-beta BMP pathways. Stimulation Smad4-deficient with 1 or BMP-7 in absence presence exogenous Smad4, followed by cDNA microarray analysis, revealed 173 mostly Smad4-dependent, TGF-beta-, BMP-responsive genes. Among...

10.1128/mcb.24.10.4241-4254.2004 article EN Molecular and Cellular Biology 2004-04-30
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