Publications
Detailed Information
Inhibitor of differentiation 4 drives brain tumor-initiating cell genesis through cyclin E and notch signaling
Cited 93 time in
Web of Science
Cited 99 time in Scopus
- Authors
- Issue Date
- 2008-08-05
- Publisher
- Cold Spring Harbor Laboratory Press
- Citation
- Genes Dev. 22(15): 2028-2033
- Keywords
- Animals ; Astrocytes/cytology/*physiology ; Calcium-Binding Proteins/metabolism ; Cell Culture Techniques ; Cell Line, Tumor ; Cells, Cultured ; Cerebral Cortex/cytology ; Cyclin E/*metabolism ; Glioblastoma/pathology ; Humans ; Inhibitor of Differentiation Proteins/*metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; RNA, Messenger/metabolism ; Receptor, Notch1/genetics/*metabolism ; Signal Transduction/genetics/*physiology ; Cell Transformation, Neoplastic
- Abstract
- Cellular origins and genetic factors governing the genesis and maintenance of glioblastomas (GBM) are not well understood. Here, we report a pathogenetic role of the developmental regulator Id4 (inhibitor of differentiation 4) in GBM. In primary murine Ink4a/Arf(-/-) astrocytes, and human glioma cells, we provide evidence that enforced Id4 can drive malignant transformation by stimulating increased cyclin E to produce a hyperproliferative profile and by increased Jagged1 expression with Notch1 activation to drive astrocytes into a neural stem-like cell state. Thus, Id4 plays an integral role in the transformation of astrocytes via its combined actions on two-key cell cycle and differentiation regulatory molecules.
- ISSN
- 0890-9369 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18676808
http://genesdev.cshlp.org/content/22/15/2028.full.pdf
https://hdl.handle.net/10371/67471
- Files in This Item:
- There are no files associated with this item.
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.