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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter
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Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter

机译：缺乏menin的转录因子JunD从生长抑制因子转变为生长促进因子

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摘要

Different components of the AP1 transcription factor complex appear to have distinct effects on cell proliferation and transformation. In contrast to other AN components, JwunD has been shown to inhibit cell proliferation. Also, in prior studies, JunD alone bound menin, product of the MEN1 tumor suppressor gene, and JunD's transcriptional activity was inhibited by menin, suggesting that JunD might achieve all or most of its unique properties through binding to menin. Analyses of JunD and menin effects on proliferation, morphology, and cyclin D1 in stable cell lines unmasked an unexpected growth promoting activity of JunD. Whereas stable overexpression of wild-type (wt) mouse JunD in JunD(-/-) immortalized fibroblasts inhibited their proliferation and reverted their transformed-like phenotype, overexpression of a missense mouse JunD mutant (mJunD(G42E)) with disabled binding to menin showed opposite or growth promoting effects. Similarly, stable overexpression of wt mouse JunD in wt immortalized fibroblasts inhibited growth. In contrast, its overexpression in Men1(-/-) immortalized fibroblasts enhanced their already transformed-like characteristics. To conclude, JunD changed from growth suppressor to growth promoter when its binding to menin was prevented by a JunD mutant unable to bind menin or by Men1-null genetic background. [References: 31]
机译：AP1转录因子复合物的不同成分似乎对细胞增殖和转化具有独特的影响。与其他AN组分相反，JwunD已显示出抑制细胞增殖的作用。同样，在以前的研究中，JunD单独结合了Men1抑癌基因的产物menin，而MenD抑制了JunD的转录活性，这表明JunD可能通过与menin结合来实现其全部或大部分独特特性。 JunD和Menin对稳定细胞系中增殖，形态和细胞周期蛋白D1的影响的分析揭示了JunD出乎意料的促进生长的活性。尽管在JunD（-/-）永生化成纤维细胞中野生型（wt）小鼠JunD的稳定过表达抑制了它们的增殖并恢复了其转化样的表型，但是错义的小鼠JunD突变体（mJunD（G42E））的过表达却与Menin的结合被禁用显示相反或促进生长的作用。同样，wt永生化成纤维细胞中wt小鼠JunD的稳定过表达抑制了生长。相反，它在Men1（-/-）永生化成纤维细胞中的过表达增强了它们已经转化的特征。总而言之，当无法结合Menin的JunD突变体或Men1-null遗传背景阻止了JunD与menin的结合时，JunD从生长抑制物变为生长促进剂。 [参考：31]

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