Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due toNORAD’s extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function ofNORADin different BC subtypes and howNORADimpacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2,NORADhas been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently,NORADhas been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network ofNORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment.
DNA损伤激活的长链非编码RNA(NORAD)近期被发现与癌症进展的病理机制相关。由于NORAD具有广泛的相互作用分子,其在乳腺癌中作为致癌基因或抑癌基因的作用存在矛盾数据。本综述将总结NORAD在不同乳腺癌亚型中的功能,及其如何影响该病理过程中的关键信号通路。研究显示,NORAD通过优先结合Pumilio蛋白PUM1和PUM2,参与调控细胞周期、血管生成、有丝分裂、DNA复制与转录以及蛋白质翻译过程。最新证据表明,NORAD还能通过与其他非编码RNA、信使RNA及蛋白质相互作用,发挥不依赖于PUM蛋白的功能。NORAD介导的信号通路复杂网络,可能为设计新型策略以克服乳腺癌化疗耐药性提供新的思路。
NORAD-Regulated Signaling Pathways in Breast Cancer Progression