Interferon-induced revertants of ras-transformed cells: resistance to transformation by specific oncogenes and retransformation by 5-azacytidine.

AUTOR(ES)

Samid, D

RESUMO

Prolonged alpha/beta interferon (IFN-alpha/beta) treatment of NIH 3T3 cells transformed by a long terminal repeat-activated Ha-ras proto-oncogene resulted in revertants that maintained a nontransformed phenotype long after IFN treatment had been discontinued. Cloned persistent revertants (PRs) produced large amounts of the ras-encoded p21 and were refractile to transformation by EJras DNA and by transforming retroviruses which carried the v-Ha-ras, v-Ki-ras, v-abl, or v-fes oncogene. Transient treatment either in vitro or in vivo with cytidine analogs that alter gene expression by inhibiting DNA methylation resulted in transformation of PR, but not of NIH 3T3, cells. The PR retransformants reverted again with IFN, suggesting that DNA methylation is involved in IFN-induced persistent reversion.

Documentos Relacionados

• Resistance to oncogenic transformation in revertant R1 of human ras-transformed NIH 3T3 cells.
• Rho-stimulated Contractility Contributes to the Fibroblastic Phenotype of Ras-transformed Epithelial Cells
• Short-term treatment with gamma interferon induces stable reversion of ras-transformed mouse fibroblasts.
• Resistance to Virus Infection Conferred by the Interferon-Induced Promyelocytic Leukemia Protein
• Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid