Nodal/Activin Signaling Drives Self-Renewal and Tumorigenicity of Pancreatic Cancer Stem Cells and Provides a Target for Combined Drug Therapy
2012; Elsevier BV; Volume: 10; Issue: 1 Linguagem: Inglês
10.1016/j.stem.2011.12.001
ISSN1934-5909
AutoresEnza Lonardo, Patrick Hermann, M Mueller, Stephan M. Huber, Anamaria Balic, Irene Miranda‐Lorenzo, Sladjana Zagorac, Sonia Alcalá, Iker Rodríguez-Arabaolaza, Juan Carlos Ramírez, Raúl Torres, Elena Cano García, Manuel Hidaldo, David Cebrián, Rainer Heuchel, Matthias Löhr, Frank Berger, Peter Bartenstein, Alexandra Aicher, Christopher Heeschen,
Tópico(s)Cancer Research and Treatments
Resumo(Cell Stem Cell 9, 433–446, November 4, 2011) The supplemental information file originally published with this article inadvertently showed Figure S6 in the place of Figure S4. A corrected version has now been posted online in its place. We apologize for any confusion caused. Nodal/Activin Signaling Drives Self-Renewal and Tumorigenicity of Pancreatic Cancer Stem Cells and Provides a Target for Combined Drug TherapyLonardo et al.Cell Stem CellNovember 04, 2011In BriefNodal and Activin belong to the TGF-β superfamily and are important regulators of embryonic stem cell fate. Here we investigated whether Nodal and Activin regulate self-renewal of pancreatic cancer stem cells. Nodal and Activin were hardly detectable in more differentiated pancreatic cancer cells, while cancer stem cells and stroma-derived pancreatic stellate cells markedly overexpressed Nodal and Activin, but not TGF-β. Knockdown or pharmacological inhibition of the Nodal/Activin receptor Alk4/7 in cancer stem cells virtually abrogated their self-renewal capacity and in vivo tumorigenicity, and reversed the resistance of orthotopically engrafted cancer stem cells to gemcitabine. Full-Text PDF Open Archive
Referência(s)