Expression of the high mobility group A family member p8 is essential to maintaining tumorigenic potential by promoting cell cycle dysregulation in LβT2 cells
| Autor: | C. M. Million Passe, K. M. Brannon, Christine C. Quirk, Michael W. King, Crystal R. White, N. A. Bade |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
endocrine system Cancer Research Time Factors Blotting Western Population Gene Expression Mice Nude Biology medicine.disease_cause Resting Phase Cell Cycle Mice medicine Animals education Cyclin-Dependent Kinase Inhibitor p57 Cellular Senescence Cell Line Transformed Cell Proliferation Oligonucleotide Array Sequence Analysis HMGA Proteins education.field_of_study Mutation Reverse Transcriptase Polymerase Chain Reaction Cell growth Cell Cycle G1 Phase HMGA Neoplasms Experimental Cell cycle beta-Galactosidase Phenotype Neoplasm Proteins Cell biology DNA-Binding Proteins Oncology Cell culture Carcinogenesis Cyclin-Dependent Kinase Inhibitor p27 |
| Zdroj: | Cancer Letters. 254:146-155 |
| ISSN: | 0304-3835 |
| DOI: | 10.1016/j.canlet.2007.03.011 |
| Popis: | The mechanism by which the HMGA protein p8 facilitates tumorigenesis may be cell cycle dysregulation. Control- (C) LbetaT2 cells, which express p8, form tumors at a rate five-times faster than p8-knockdown (p8-KD)-LbetaT2 cells. In association with this heightened tumorigenic potential, p8-expressing C-LbetaT2 cells avoid G(0)/G(1) arrest and become genetically unstable while p8-KD-LbetaT2 cells arrest in G(0)/G(1), become senescent upon overgrowth, and maintain a diploid population. These phenotypic changes correspond to altered cell cycle regulation at the G(1)-to-S transition that may be due to p8-mediated changes in expression of the Cip/Kip family members of cell cycle inhibitors, p21, p27, and p57. |
| Databáze: | OpenAIRE |
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