دورية أكاديمية
أعرض في EDS

Androgen receptor and MYC equilibration centralizes on developmental super-enhancer.

التفاصيل البيبلوغرافية
العنوان: Androgen receptor and MYC equilibration centralizes on developmental super-enhancer.
المؤلفون: Guo H; Department of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033,, Shandong, China.; Shandong Engineering & Technology Research Center for Tumor Marker Detection, Jinan, 250033,, Shandong, China.; Shandong Provincial Clinical Medicine Research Center for Clinical Laboratory, Jinan, 250033,, Shandong, China., Wu Y; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.; Institutes of Biomedical Sciences, Fudan University, Shanghai, 200433, China., Nouri M; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA., Spisak S; Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, 02215, USA., Russo JW; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA., Sowalsky AG; Laboratory of Genitourinary Cancer Pathogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA., Pomerantz MM; Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA., Wei Z; Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China., Korthauer K; Department of Statistics, University of British Columbia, Vancouver, BC, Canada., Seo JH; Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA., Wang L; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA., Arai S; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.; Department of Urology, Gunma University Hospital, Maebashi, Gunma, Japan., Freedman ML; Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.; The Eli and Edythe L. Broad Institute, Cambridge, MA, 02142, USA., He HH; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada. hansenhe@uhnresearch.ca.; Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada. hansenhe@uhnresearch.ca., Chen S; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA. schen@bidmc.harvard.edu., Balk SP; Hematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA. sbalk@bidmc.harvard.edu.
المصدر: Nature communications [Nat Commun] 2021 Dec 15; Vol. 12 (1), pp. 7308. Date of Electronic Publication: 2021 Dec 15.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Enhancer Elements, Genetic*, Oncogene Protein p55(v-myc)/*genetics , Receptors, Androgen/*genetics, Androgens/metabolism ; Cell Line, Tumor ; Chromatin/genetics ; Chromatin/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Oncogene Protein p55(v-myc)/metabolism ; Promoter Regions, Genetic ; Prostatic Neoplasms/metabolism ; Receptors, Androgen/metabolism ; Signal Transduction
مستخلص: Androgen receptor (AR) in prostate cancer (PCa) can drive transcriptional repression of multiple genes including MYC, and supraphysiological androgen is effective in some patients. Here, we show that this repression is independent of AR chromatin binding and driven by coactivator redistribution, and through chromatin conformation capture methods show disruption of the interaction between the MYC super-enhancer within the PCAT1 gene and the MYC promoter. Conversely, androgen deprivation in vitro and in vivo increases MYC expression. In parallel, global AR activity is suppressed by MYC overexpression, consistent with coactivator redistribution. These suppressive effects of AR and MYC are mitigated at shared AR/MYC binding sites, which also have markedly higher levels of H3K27 acetylation, indicating enrichment for functional enhancers. These findings demonstrate an intricate balance between AR and MYC, and indicate that increased MYC in response to androgen deprivation contributes to castration-resistant PCa, while decreased MYC may contribute to responses to supraphysiological androgen therapy.
(© 2021. The Author(s).)
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معلومات مُعتمدة: P50 CA090381 United States CA NCI NIH HHS; R00 CA135592 United States CA NCI NIH HHS; U54 CA156732 United States CA NCI NIH HHS; K99 CA135592 United States CA NCI NIH HHS; P01 CA163227 United States CA NCI NIH HHS; R01 CA251555 United States CA NCI NIH HHS; R01 CA193910 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Androgens)
0 (Chromatin)
0 (Oncogene Protein p55(v-myc))
0 (Receptors, Androgen)
تواريخ الأحداث: Date Created: 20211216 Date Completed: 20220118 Latest Revision: 20220716
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8674345
DOI: 10.1038/s41467-021-27077-y
PMID: 34911936
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-021-27077-y