Data from Identification of a Cyclin D1 Network in Prostate Cancer That Antagonizes Epithelial–Mesenchymal Restraint

التفاصيل البيبلوغرافية
العنوان: Data from Identification of a Cyclin D1 Network in Prostate Cancer That Antagonizes Epithelial–Mesenchymal Restraint
المؤلفون: Richard G. Pestell, Adam Ertel, Michael P. Lisanti, Andrew A. Quong, Min Wang, Ke Chen, Marco Crosariol, Sanjay Katiyar, Xuanmao Jiao, Hui Meng, Michael Gormley, Mathew C. Casimiro, Xiaoming Ju
بيانات النشر: American Association for Cancer Research (AACR), 2023.
سنة النشر: 2023
الوصف: Improved clinical management of prostate cancer has been impeded by an inadequate understanding of molecular genetic elements governing tumor progression. Gene signatures have provided improved prognostic indicators of human prostate cancer. The TGF-β/BMP-SMAD4 signaling pathway, which induces epithelial–mesenchymal transition (EMT), is known to constrain prostate cancer progression induced by Pten deletion. Herein, cyclin D1 inactivation reduced cellular proliferation in the murine prostate in vivo and in isogenic oncogene–transformed prostate cancer cell lines. The in vivo cyclin D1–mediated molecular signature predicted poor outcome of recurrence-free survival for patients with prostate cancer (K-means HR, 3.75, P = 0.02) and demonstrated that endogenous cyclin D1 restrains TGF-β, Snail, Twist, and Goosecoid signaling. Endogenous cyclin D1 enhanced Wnt and ES cell gene expression and expanded a prostate stem cell population. In chromatin immunoprecipitation sequencing, cyclin D1 occupied genes governing stem cell expansion and induced their transcription. The coordination of EMT restraining and stem cell expanding gene expression by cyclin D1 in the prostate may contribute to its strong prognostic value for poor outcome in biochemical-free recurrence in human prostate cancer. Cancer Res; 74(2); 508–19. ©2013 AACR.
DOI: 10.1158/0008-5472.c.6505917
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::fe2cce317a933f60f8c15ffc530cb450
https://doi.org/10.1158/0008-5472.c.6505917
Rights: OPEN
رقم الانضمام: edsair.doi...........fe2cce317a933f60f8c15ffc530cb450
قاعدة البيانات: OpenAIRE
الوصف
DOI:10.1158/0008-5472.c.6505917