BACKGROUND The key oncogene B-cell lymphoma 6 (BCL6) drives malignant progression by promoting proliferation, overriding DNA damage checkpoints and blocking cell terminal differentiation. However, its functions in the placenta and the endometrium remain to be defined. OBJECTIVE AND RATIONALE Recent studies provide evidence that BCL6 may play various roles in the human placenta and the endometrium. Deregulated BCL6 might be related to the pathogenesis of pre-eclampsia (PE) as well as endometriosis. In this narrative review, we aimed to summarize the current knowledge regarding the pathophysiological role of BCL6 in these two reproductive organs, discuss related molecular mechanisms, and underline associated research perspectives. SEARCH METHODS We conducted a comprehensive literature search using PubMed for human, animal and cellular studies published until October 2021 in the following areas: BCL6 in the placenta, in PE and in endometriosis, in combination with its functions in proliferation, fusion, migration, invasion, differentiation, stem/progenitor cell maintenance and lineage commitment. OUTCOMES The data demonstrate that BCL6 is important in cell proliferation, survival, differentiation, migration and invasion of trophoblastic cells. BCL6 may have critical roles in stem/progenitor cell survival and differentiation in the placenta and the endometrium. BCL6 is aberrantly upregulated in pre-eclamptic placentas and endometriotic lesions through various mechanisms, including changes in gene transcription and mRNA translation as well as post-transcriptional/translational modifications. Importantly, increased endometrial BCL6 is considered to be a non-invasive diagnostic marker for endometriosis and a predictor for poor outcomes of IVF. These data highlight that BCL6 is crucial for placental development and endometrium homeostasis, and its upregulation is associated with the pathogenesis of PE, endometriosis and infertility. WIDER IMPLICATIONS The lesson learned from studies of the key oncogene BCL6 reinforces the notion that numerous signaling pathways and regulators are shared by tumors and reproductive organs. Their alteration may promote the progression of malignancies as well as the development of gestational and reproductive disorders.

中文翻译：

---

BCL6，胎盘、先兆子痫和子宫内膜异位症中的关键致癌基因

背景关键致癌基因 B 细胞淋巴瘤 6 (BCL6) 通过促进增殖、超越 DNA 损伤检查点和阻断细胞终末分化来驱动恶性进展。然而，其在胎盘和子宫内膜中的功能仍有待确定。目的和基本原理 最近的研究提供的证据表明 BCL6 可能在人类胎盘和子宫内膜中发挥多种作用。BCL6 失调可能与先兆子痫 (PE) 和子宫内膜异位症的发病机制有关。在这篇叙述性综述中，我们旨在总结当前关于 BCL6 在这两个生殖器官中的病理生理学作用的知识，讨论相关的分子机制，并强调相关的研究观点。搜索方法 我们使用 PubMed 对人类、截至 2021 年 10 月在以下领域发表的动物和细胞研究：胎盘、PE 和子宫内膜异位症中的 BCL6，结合其在增殖、融合、迁移、侵袭、分化、干细胞/祖细胞维持和谱系定型中的功能。结果 数据表明 BCL6 在滋养层细胞的细胞增殖、存活、分化、迁移和侵袭中很重要。BCL6 可能在胎盘和子宫内膜的干/祖细胞存活和分化中起关键作用。BCL6 通过各种机制在先兆子痫胎盘和子宫内膜异位病变中异常上调，包括基因转录和 mRNA 翻译的变化以及转录后/翻译修饰。重要的，增加的子宫内膜 BCL6 被认为是子宫内膜异位症的非侵入性诊断标志物和 IVF 不良结果的预测因子。这些数据强调 BCL6 对胎盘发育和子宫内膜稳态至关重要，其上调与 PE、子宫内膜异位症和不孕症的发病机制有关。更广泛的意义 从对关键致癌基因 BCL6 的研究中吸取的教训强化了这样一种观念，即肿瘤和生殖器官共有许多信号通路和调节因子。它们的改变可能会促进恶性肿瘤的进展以及妊娠和生殖障碍的发展。其上调与 PE、子宫内膜异位症和不孕症的发病机制有关。更广泛的意义 从对关键致癌基因 BCL6 的研究中吸取的教训强化了这样一种观念，即肿瘤和生殖器官共有许多信号通路和调节因子。它们的改变可能会促进恶性肿瘤的进展以及妊娠和生殖障碍的发展。其上调与 PE、子宫内膜异位症和不孕症的发病机制有关。更广泛的意义 从对关键致癌基因 BCL6 的研究中吸取的教训强化了这样一种观念，即肿瘤和生殖器官共有许多信号通路和调节因子。它们的改变可能会促进恶性肿瘤的进展以及妊娠和生殖障碍的发展。