The bcl-2transcription factors in human endometrium

雌激素-雌激素受体(ER)信号通路不仅在生殖调控中发挥着重要的生理作用，而且在乳腺癌和子宫癌的发生中也起着重要的生理作用。虽然一些ER靶基因已被鉴定为含有雌激素反应元件(ERE)，但另一些基因最终是由雌激素通过蛋白质相互作用激活的，而不与ERE结合。在以前的研究中，我们发现bcl2基因在腺细胞中的增殖期特异性表达可以通过c-jun与其启动子中的基序结合来调节。目前的研究结果表明，bcl2的月经周期表达既可以由c-jun启动子中era与ERE的直接结合，也可以通过与其基序结合的c-jun的相互作用来控制。有趣的是，在Ser73处磷酸化的c-jun的转录活性形式被发现以一种非特异性的方式与所鉴定的基序结合。我们的研究揭示了一种新的机制，即在转录水平上调节bcl2在正常子宫内膜中的表达。

The estrogen-estrogen receptor (ER) signalling pathway plays crucial physiologic roles not only in control of reproduction, but also the generation of cancer in breast and uterus. While some ER target genes have been identified containing the estrogen responsive element (ERE), others are activated eventually by estrogen via protein-protein interaction without binding to ERE. In a previous study we found out that the proliferative stage-specific expression of the bcl-2 gene in the glandular cells could be regulated by binding of c-Jun to its motifs in the promoter. Results from the present studies indicate that the menstrual cyclic expression of bcl-2 could be controlled by either the direct binding of ERa to ERE in the c-jun promoter or the interaction with c-Jun that binds to its motifs in the bcl-2 gene. Intriguingly, the transcriptionally active form of c-Jun phosphorylated at Ser73 was identified binding to the identified motifs in a menstrual cycle non-specific manner. Our studies revealed a novel mechanism that transcriptionally regulates the expression of bcl-2 in normal human endometrium.