Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma

The Polycomb group and oncogene Bmi1 is required for the proliferation of various differentiated cells and for the self-renewal of stem cells and leukemic cancer stem cells. Repression of the Ink4a/Arf locus is a well described mechanism through which Bmi1 can exert its proliferative effects. Howeve...

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Veröffentlicht in:Cancer cell Jg. 12; H. 4; S. 328
Hauptverfasser: Bruggeman, Sophia W M, Hulsman, Danielle, Tanger, Ellen, Buckle, Tessa, Blom, Marleen, Zevenhoven, John, van Tellingen, Olaf, van Lohuizen, Maarten
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.10.2007
Schlagworte:
3T3 Cells
Animals
Astrocytes - metabolism
Astrocytes - pathology
Brain Neoplasms - genetics
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cell Differentiation
Cell Proliferation
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Cells, Cultured
Cyclin-Dependent Kinase Inhibitor p16 - deficiency
Cyclin-Dependent Kinase Inhibitor p16 - genetics
Cyclin-Dependent Kinase Inhibitor p16 - metabolism
Gene Expression Regulation, Neoplastic
Glioblastoma - genetics
Glioblastoma - metabolism
Glioblastoma - pathology
Mice
Mice, Inbred BALB C
Mice, Knockout
Mice, Nude
Mutation
Neoplasm Staging
Neoplasms, Experimental - metabolism
Neoplasms, Experimental - pathology
Neurons - metabolism
Neurons - pathology
Nuclear Proteins - deficiency
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Phenotype
Polycomb Repressive Complex 1
Proto-Oncogene Proteins - deficiency
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Receptor, Epidermal Growth Factor - genetics
Receptor, Epidermal Growth Factor - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
Signal Transduction - genetics
Stem Cells - metabolism
Stem Cells - pathology
Time Factors
Transduction, Genetic
ISSN:1535-6108
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Zusammenfassung:The Polycomb group and oncogene Bmi1 is required for the proliferation of various differentiated cells and for the self-renewal of stem cells and leukemic cancer stem cells. Repression of the Ink4a/Arf locus is a well described mechanism through which Bmi1 can exert its proliferative effects. However, we now demonstrate in an orthotopic transplantation model for glioma, a type of cancer harboring cancer stem cells, that Bmi1 is also required for tumor development in an Ink4a/Arf-independent manner. Tumors derived from Bmi1;Ink4a/Arf doubly deficient astrocytes or neural stem cells have a later time of onset and different histological grading. Moreover, in the absence of Ink4a/Arf, Bmi1-deficient cells and tumors display changes in differentiation capacity.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1535-6108
DOI:10.1016/j.ccr.2007.08.032