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首页> 外文期刊>EMBO Journal >MODULATION OF RETINOIC ACID SENSITIVITY IN LUNG CANCER CELLS THROUGH DYNAMIC BALANCE OF ORPHAN RECEPTORS NUR77 AND COUP-TF AND THEIR HETERODIMERIZATION
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MODULATION OF RETINOIC ACID SENSITIVITY IN LUNG CANCER CELLS THROUGH DYNAMIC BALANCE OF ORPHAN RECEPTORS NUR77 AND COUP-TF AND THEIR HETERODIMERIZATION

机译：调制的视黄酸敏感性肺肿瘤细胞通过动态平衡的孤儿受体NUR77 COUP-TF和他们HETERODIMERIZATION

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The diverse function of retinoic acid (RA) is mediated by its nuclear receptors, the retinoic acid receptors (RARs) and retinoid,X receptors (RXRs), However, the RA response is often lost in cancer cells that express the receptors, Previously, it was demonstrated that the RA response is regulated by the COUP-TF orphan receptors, Here, we present evidence that nur77, another orphan receptor whose expression is highly induced by phorbol esters and growth factors, is involved in modulation of the RA response, Expression of nur77 enhances ligand-independent transactivation of RA response elements (RAREs) and desensitizes their RA responsiveness. Conversely,;expression of COUP-TF sensitizes RA responsiveness of RAREs by repressing their basal transactivation activity;, Unlike the effect of COUP-TFs, the function of nur77 does not require direct binding of nur77 to the RAREs, but is through interaction between nur77 and COUP-TFs, The interaction occurs in solution and results in inhibition of COUP-TF RARE binding and transcriptional activity, Unlike other nuclear receptors, a large portion of the carboxy-terminal end of nur77 is not required for its interaction with COUP-TF: In human lung cancer cell lines, COUP-TF is highly expressed in RA-sensitive cell lines while nur77 expression is associated with RA resistance, Stable expression of COUP-TF in nur77-positive, RA-resistant lung cancer cells enhances the inducibility of RAR beta gene expression and growth inhibition by RA, These observations demonstrate that a dynamic equilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness of human lung cancer cells. [References: 44]
机译：维甲酸(RA)的不同功能由其核受体,视黄酸受体(rar)和类维生素a, X受体(rxr),然而,往往迷失在RA响应癌细胞表达受体,以前,证明了类风湿性关节炎反应是由COUP-TF孤儿受体,在这里,我们目前的证据表明nur77,另一个孤儿受体的表达佛波醇酯引起的高度和增长因素,参与了RA的调制反应,表达nur77增强ligand-independent transactivation RA的反应元素(罕见),逐渐脱敏RA响应性。糖分会让RA罕见的响应能力压抑他们的基底transactivation活动,COUP-TFs的影响,不同的功能nur77不需要直接绑定nur77罕见的,但是是通过互动nur77 COUP-TFs,交互发生在COUP-TF抑制的解决方案和结果罕见的绑定和转录活动,不像其他核受体的很大一部分carboxy-terminal nur77年底不是必需的其与COUP-TF互动:在人类的肺癌症细胞系,COUP-TF高度表达RA-sensitive细胞系而nur77表达式与RA阻力,稳定的表达在nur77-positive COUP-TF RA-resistant肺癌症细胞增强RAR的可诱导性β基因表达和生长抑制类风湿性关节炎,这些观察表明动态孤儿受体nur77和平衡COUP-TF,通过heterodimerization调节COUP-TF罕见的绑定,是至关重要的RA人类肺癌细胞的响应能力。(引用:44)

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