Journal
GENES & DEVELOPMENT
Volume 22, Issue 15, Pages 2028-2033Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1668708
Keywords
Id4; Ink4a/Arf(-/-) astrocyte; notch signaling; cyclin E; neural stem-like cells; glioblastoma
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Funding
- NCI NIH HHS [P01CA95616, R01CA99041, R01 CA099041, P01 CA095616] Funding Source: Medline
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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.
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