Summary: | Long non-coding RNA activated by DNA damage (<i>NORAD</i>) has recently been associated with pathologic mechanisms underlying cancer progression. Due to <i>NORAD</i>’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 of <i>NORAD</i> in different BC subtypes and how <i>NORAD</i> impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, <i>NORAD</i> has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, <i>NORAD</i> has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of <i>NORAD</i>-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment.
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