Abstract

Management of breast cancer banks upon hormone receptor (HR) status, whose absence is associated with features like poor prognosis and aneuploidy. A newly identified protein, CUEDC2 was found maintaining HR level by promoting its degradation, while its moonlighting job is detected in ploidy maintenance during mitosis. The HR members (ER/PR) function as transcription factors. However, their involvement in transregulation of mitotic checkpoint protein(s) is largely unexplored. We hypothesize that HR controls mitosis and maintains ploidy by employing its transregulatory activity, while upregulated CUEDC2, as seen in several cancer types, rendering HR reduction, promotes mitotic deregulation and aneuploidy in HR-negative breast cancer.

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