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Reconstitution of TGFBR2-Mediated Signaling Causes Upregulation of GDF-15 in HCT116 Colorectal Cancer Cells.

Abstract
Although inactivating frameshift mutations in the Transforming growth factor beta receptor type 2 (TGFBR2) gene are considered as drivers of microsatellite unstable (MSI) colorectal tumorigenesis, consequential alterations of the downstream target proteome are not resolved completely. Applying a click-it chemistry protein labeling approach combined with mass spectrometry in a MSI colorectal cancer model cell line, we identified 21 de novo synthesized proteins differentially expressed upon reconstituted TGFBR2 expression. One candidate gene, the TGF-ß family member Growth differentiation factor-15 (GDF-15), exhibited TGFBR2-dependent transcriptional upregulation causing increased intracellular and extracellular protein levels. As a new TGFBR2 target gene it may provide a link between the TGF-ß branch and the BMP/GDF branch of SMAD-mediated signaling.
AuthorsJennifer Lee, Fabia Fricke, Uwe Warnken, Martina Schnölzer, Jürgen Kopitz, Johannes Gebert
JournalPloS one (PLoS One) Vol. 10 Issue 6 Pg. e0131506 ( 2015) ISSN: 1932-6203 [Electronic] United States
PMID26114631 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • GDF15 protein, human
  • Growth Differentiation Factor 15
  • Receptors, Transforming Growth Factor beta
  • Smad Proteins
  • Protein Serine-Threonine Kinases
  • Receptor, Transforming Growth Factor-beta Type II
Topics
  • Colorectal Neoplasms (genetics, metabolism, pathology)
  • Gene Expression Regulation, Neoplastic (drug effects)
  • Growth Differentiation Factor 15 (genetics, metabolism, pharmacology)
  • HCT116 Cells
  • Humans
  • Protein Serine-Threonine Kinases (genetics, physiology)
  • Receptor, Transforming Growth Factor-beta Type II
  • Receptors, Transforming Growth Factor beta (genetics, physiology)
  • Signal Transduction (drug effects, genetics)
  • Smad Proteins (metabolism)
  • Transcriptional Activation (genetics)
  • Up-Regulation (drug effects, genetics)

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