Further characterization of retinoblastoma gene-mediated cell growth and tumor suppression in human cancer cells.
AUTOR(ES)
Zhou, Y
RESUMO
We have transfected the osteosarcoma cell line Saos2 and the bladder carcinoma cell line 5637 with additional retinoblastoma (RB) expression plasmids. The RB-reconstituted Saos2 and 5637 cells showed only slightly lower ratios of cells undergoing DNA synthesis compared to their parental RB- tumor cells, and there were no noticeable changes in cell morphology. Furthermore, we have isolated long-term RB+ clones from Saos2, 5637, and the retinoblastoma cell line WERI-Rb27 after transfection/transduction with a RB expression plasmid or retrovirus. These clones were similar to their parental cell lines in terms of morphology and growth rates, and they all expressed functional RB protein (p110RB) as evidenced by its potential of phosphorylation, simian virus 40 large tumor antigen binding, and nuclear tethering. No mutation or deletion of the exogenous RB gene was detectable by PCR and single-strand conformation polymorphism analysis. In addition, either the individual or pooled RB+ clones did form malignant tumors in nude mice but usually with a longer latency period and lower frequency. Such tumors also retained normal RB expression, suggesting that at least a portion of the RB-reconstituted tumor cells were still tumorigenic. This phenomenon is referred to by us as tumor suppressor resistance (TSR).
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=43745Documentos Relacionados
- B-myb Promoter Retargeting of Herpes Simplex Virus γ34.5 Gene-Mediated Virulence toward Tumor and Cycling Cells
- The retinoblastoma gene functions as a growth and tumor suppressor in human bladder carcinoma cells.
- Envelope Gene-Mediated Neurovirulence in Feline Immunodeficiency Virus Infection: Induction of Matrix Metalloproteinases and Neuronal Injury
- Analysis of a tobacco mosaic virus strain capable of overcoming N gene-mediated resistance.
- Arabidopsis RAR1 Exerts Rate-Limiting Control of R Gene–Mediated Defenses against Multiple Pathogens