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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Overexpression of the c-Myc oncoprotein blocks the growth-inhibitory response but is required for the mitogenic effects of transforming growth factor beta 1.
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Overexpression of the c-Myc oncoprotein blocks the growth-inhibitory response but is required for the mitogenic effects of transforming growth factor beta 1.

机译：c-Myc癌蛋白的过表达会阻止生长抑制反应，但对于转化生长因子beta 1的促有丝分裂作用是必需的。

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摘要

One of the more intriguing aspects of transforming growth factor beta 1 (TGF beta 1) is its ability to function as both a mitogenic factor for certain mesenchymal cells and a potent growth inhibitor of lymphoid, endothelial, and epithelial cells. Data are presented indicating that c-myc may play a pivotal role in both the mitogenic and antiproliferative actions of TGF beta 1. In agreement with previous studies using C3H/10T1/2 fibroblasts constitutively expressing an exogenous c-myc cDNA, we show that AKR-2B fibroblasts expressing a chimeric estrogen-inducible form of c-myc (mycER) are able to form colonies in soft agar in the presence of TGF beta 1 only when c-myc is activated by hormone. Whereas these findings support a synergistic role for c-myc in mitogenic responses to TGF beta 1, we also find that c-myc can antagonize the growth-inhibitory response to TGF beta 1. Mouse keratinocytes (BALB/MK), which are normally growth-arrested by TGF beta 1, are rendered insensitive to the growth-inhibitory effects of TGF beta 1 upon mycER activation. This ability of mycER activation to block TGF beta 1-induced growth arrest was found to occur only when the fusion protein was induced with hormone in the early part of G1. Addition of estradiol late in G1 had no suppressive effect on TGF beta 1-induced growth inhibition.
机译：转化生长因子beta 1（TGF beta 1）更具吸引力的方面之一是它既可以充当某些间充质细胞的促有丝分裂因子，又可以有效地抑制淋巴，内皮和上皮细胞的生长。提供的数据表明c-myc可能在TGF beta 1的促有丝分裂和抗增殖作用中都起着关键作用。与以前使用组成型表达外源性c-myc cDNA的C3H / 10T1 / 2成纤维细胞的研究一致，我们证明了AKR仅当c-myc被激素激活时，表达嵌合雌激素诱导形式的c-myc（mycER）的-2B成纤维细胞才能够在TGF beta 1存在的情况下在软琼脂中形成菌落。尽管这些发现支持c-myc在对TGFβ1的促有丝分裂反应中具有协同作用，但我们还发现c-myc可以拮抗对TGF beta 1的生长抑制反应。小鼠角质形成细胞（BALB / MK），通常是生长的-被TGF beta 1阻止-对mycER激活后的TGF beta 1的生长抑制作用不敏感。发现只有在G1早期用激素诱导融合蛋白时，才会发生mycER激活阻断TGFβ1诱导的生长停滞的能力。在G1晚期添加雌二醇对TGFβ1诱导的生长抑制没有抑制作用。

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