Expression of an exogenous eukaryotic DNA methyltransferase gene induces transformation of NIH 3T3 cells.
AUTOR(ES)
Wu, J
RESUMO
Abnormal regional increases in DNA methylation, which have potential for causing gene inactivation and chromosomal instability, are consistently found in immortalized and tumorigenic cells. Increased DNA methyltransferase activity, which is also a characteristic of such cells, is a candidate to mediate these abnormal DNA methylation patterns. We now show that, in NIH 3T3 mouse fibroblasts, constitutive overexpression of an exogenous mouse DNA methyltransferase gene results in a marked increase in overall DNA methylation which is accompanied by tumorigenic transformation. These transformation changes can also be elicited by dexamethasone-inducible expression of an exogenous DNA methyltransferase gene. Our findings provide strong evidence that the increase in DNA methyltransferase activity associated with tumor progression could be a key step in carcinogenesis and provide a model system that can be used to further study this possibility.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=47466Documentos Relacionados
- Mutated alpha subunit of the Gq protein induces malignant transformation in NIH 3T3 cells.
- Human papillomavirus type 16 DNA-induced malignant transformation of NIH 3T3 cells.
- Transformation of human cells by DNAs ineffective in transformation of NIH 3T3 cells.
- Transformation of NIH 3T3 cells by DNA of the MCF-7 human mammary carcinoma cell line induces expression of an endogenous murine leukemia provirus.
- High-level expression of human insulin receptor cDNA in mouse NIH 3T3 cells.
