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- W2068754616 abstract "The incidence of endometrial cancer is on the rise; it is the fourth most common gynecological malignancy in the United States with an estimated diagnosis for 2013 of 49 470 (American Cancer Society). Endometrial adenocarcinoma type I (endometrioid histology) is etiologically linked to unopposed estrogen (anovulation [lack of progesterone], hormone therapy), causing uncontrolled proliferation marked by loss of the cyclin-dependent kinase inhibitor, p27kip1 (p27), a potent inducer of cell-cycle arrest. Previously, Gold and colleagues (1) had shown that estrogen destroys and progesterone prevents destruction of nuclear p27 solely through manipulation of the ubiquitin-proteasome system (UPS). Therefore, the major ovarian steroids, estrogen and progesterone, hijack UPS service to regulate the stabilization of p27 for growth stimulation or inhibition, respectively. These studies established the prevention of estrogen-induced p27 destruction as an important molecular therapeutic target for endometrial cancer. Moreover, nuclear p27 is already absent in atypical endometrial hyperplasia, which precedes endometrial cancer and thus blocks p27 proteasomal degradation in the nucleus, possibly preventing the neoplastic progression. In this issue of Endocrinology, Pavlides et al (2) establish in a physiologically relevant targeting lineup, the proven specific activity for Skp2 E3ligase activity in the pocket formed by Skp2 and Cks1, whereby p27 is ubiquitylated and subsequently degraded by the UPS, thus paving the way for targeted therapy of endometrial and perhaps other cancers where p27 degradation is unchecked. To place this significant discovery in context, it is important to review the UPS cellular action and recent hallmark studies closely in targeting this system toward development of novel cancer therapeutics." @default.
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- W2068754616 date "2013-11-01" @default.
- W2068754616 modified "2023-09-27" @default.
- W2068754616 title "p27 Stands-Up-To-Cancer: UPS Nuclear Service Stops" @default.
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- W2068754616 doi "https://doi.org/10.1210/en.2013-1873" @default.
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