Regulatory mechanism of expression of ETS transcription factor Myeloid elf-1-like factor (MEF) by tumor suppressors

髓系精灵-1样因子(MEF)是一种转录因子，在发育、细胞分化、增殖、转化和免疫反应中发挥重要作用。在本研究中，我们旨在确定几种细胞因子对MEF表达的调节机制。首先，我们证明了肿瘤抑制因子P53通过诱导E3泛素连接酶MDM2的转录来降低MEF蛋白的水平。此外，研究结果还显示，另一种肿瘤抑制药Rb可能通过稳定MEF的蛋白表达来提高MEF的蛋白水平。最后，我们的数据进一步表明，低氧通过低氧的主要效应分子HIF1α增加MEF的mRNA和蛋白水平。总体而言，这些研究中的发现有助于更好地理解转录调控因子MEF是如何受到肿瘤抑制因子如p53和Rb以及缺氧相关蛋白HIF1α的影响的。

Myeloid elf-1-like factor (MEF) functions as transcriptional factor and plays critical roles in development, cellular differentiation, proliferation, transformation and immune responses. In the present study, we aim to determine the regulatory mechanisms of MEF expression by several cellular factors. First, we demonstrated that tumor suppressor p53 decreases the level of MEF protein through the induction of transcription of MDM2, an E3 ubiquitin ligase. Moreover, the findings also revealed that another tumor suppressor Rb increases the MEF protein level possibly by stabilizing its protein expression. Finally, our data further showed that hypoxia increases both the mRNA and protein levels of MEF through HIF1alpha, the main effector molecule of hypoxia. On the whole, the findings revealed in these studies provide a better understanding of how the transcriptional regulator MEF is influenced by tumor suppressors such as p53 and Rb, and by hypoxia-related protein HIF1alpha.