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首页> 外文期刊>Molecular and Cellular Biology >Interferon-induced revertants of ras-transformed cells: resistance to transformation by specific oncogenes and retransformation by 5-azacytidine.
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Interferon-induced revertants of ras-transformed cells: resistance to transformation by specific oncogenes and retransformation by 5-azacytidine.

机译：干扰素诱导的RAS转化细胞的恢复剂：通过特异性癌变胶和通过5-氮杂胞苷的重新形成转化的抗性。

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摘要

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.
机译：延长α/β干扰素（IFN-alpha /β）处理由长末端重复活化的HA-Ras原癌基因转化的NIH 3T3细胞导致恢复剂，其在IFN处理已经停止后保持不转化的表型。克隆持续回复剂（PRS）产生了大量的RAS编码的P21，并通过EJRAS DNA拒绝转化，并通过转化携带V-HA-RAS，V-KI-RAS，V-ABL或V-FES的逆转录病毒oncogene。瞬态治疗在体外或体内具有胞苷类似物，即通过抑制DNA甲基化改变基因表达导致Pr的转化，但不含NIH 3T3，细胞。 PR重塑剂再次用IFN再次恢复，表明DNA甲基化涉及IFN诱导的持续逆转。

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