دورية أكاديمية
أعرض في EDS

CBP loss cooperates with PTEN haploinsufficiency to drive prostate cancer: implications for epigenetic therapy.

التفاصيل البيبلوغرافية
العنوان: CBP loss cooperates with PTEN haploinsufficiency to drive prostate cancer: implications for epigenetic therapy.
المؤلفون: Ding L; Authors' Affiliations: Departments of Biochemistry and Molecular Biology, Urology, and Biomedical Statistics and Informatics, Mayo Clinic Cancer Center, and Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester; Masonic Cancer Center; Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota; Astar Biotech LLC, Richmond, Virginia; Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and College of Life Sciences, Nanjing Normal University, Nanjing, China., Chen S, Liu P, Pan Y, Zhong J, Regan KM, Wang L, Yu C, Rizzardi A, Cheng L, Zhang J, Schmechel SC, Cheville JC, Van Deursen J, Tindall DJ, Huang H
المصدر: Cancer research [Cancer Res] 2014 Apr 01; Vol. 74 (7), pp. 2050-61. Date of Electronic Publication: 2014 Feb 03.
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: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1538-7445 (Electronic) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, Md. : American Association for Cancer Research
Original Publication: Chicago [etc.]
مواضيع طبية MeSH: Epigenesis, Genetic* , Haploinsufficiency*, PTEN Phosphohydrolase/*genetics , Peptide Fragments/*physiology , Prostatic Neoplasms/*genetics , Sialoglycoproteins/*physiology, Animals ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Enhancer of Zeste Homolog 2 Protein ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Indoles/pharmacology ; Male ; Membrane Proteins/physiology ; Mice ; PTEN Phosphohydrolase/physiology ; Panobinostat ; Peptide Fragments/genetics ; Phosphoproteins/physiology ; Polycomb Repressive Complex 2/physiology ; Prostatic Neoplasms/therapy ; Proto-Oncogene Proteins c-akt/physiology ; Sialoglycoproteins/genetics ; ras GTPase-Activating Proteins/genetics
مستخلص: Despite the high incidence and mortality of prostate cancer, the etiology of this disease is not fully understood. In this study, we develop functional evidence for CBP and PTEN interaction in prostate cancer based on findings of their correlate expression in the human disease. Cbp(pc-/-);Pten(pc+/-) mice exhibited higher cell proliferation in the prostate and an early onset of high-grade prostatic intraepithelial neoplasia. Levels of EZH2 methyltransferase were increased along with its Thr350 phosphorylation in both mouse Cbp(-/-); Pten(+/-) and human prostate cancer cells. CBP loss and PTEN deficiency cooperated to trigger a switch from K27-acetylated histone H3 to K27-trimethylated bulk histones in a manner associated with decreased expression of the growth inhibitory EZH2 target genes DAB2IP, p27(KIP1), and p21(CIP1). Conversely, treatment with the histone deacetylase inhibitor panobinostat reversed this switch, in a manner associated with tumor suppression in Cbp(pc-/-);Pten(pc+/-) mice. Our findings show how CBP and PTEN interact to mediate tumor suppression in the prostate, establishing a central role for histone modification in the etiology of prostate cancer and providing a rationale for clinical evaluation of epigenetic-targeted therapy in patients with prostate cancer.
(©2014 AACR.)
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معلومات مُعتمدة: CA091956 United States CA NCI NIH HHS; CA134514 United States CA NCI NIH HHS; P30 CA015083 United States CA NCI NIH HHS; CA130908 United States CA NCI NIH HHS; P50 CA091956 United States CA NCI NIH HHS; R01 CA130908 United States CA NCI NIH HHS; R01 CA134514 United States CA NCI NIH HHS
المشرفين على المادة: 0 (CDKN1B protein, human)
0 (DAB2IP protein, human)
0 (Histones)
0 (Hydroxamic Acids)
0 (Indoles)
0 (Membrane Proteins)
0 (Pag1 protein, mouse)
0 (Peptide Fragments)
0 (Phosphoproteins)
0 (Sialoglycoproteins)
0 (bone sialoprotein (35-62), human)
0 (ras GTPase-Activating Proteins)
147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
9647FM7Y3Z (Panobinostat)
EC 2.1.1.43 (EZH2 protein, human)
EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
EC 2.1.1.43 (Polycomb Repressive Complex 2)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 3.1.3.67 (PTEN Phosphohydrolase)
تواريخ الأحداث: Date Created: 20140205 Date Completed: 20140607 Latest Revision: 20220317
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC3975662
DOI: 10.1158/0008-5472.CAN-13-1659
PMID: 24491799
قاعدة البيانات: MEDLINE
الوصف
تدمد:1538-7445
DOI:10.1158/0008-5472.CAN-13-1659