دورية أكاديمية

Scaffold dependent histone deacetylase (HDAC) inhibitor induced re-equilibration of the subcellular localization and post-translational modification state of class I HDACs.

التفاصيل البيبلوغرافية
العنوان: Scaffold dependent histone deacetylase (HDAC) inhibitor induced re-equilibration of the subcellular localization and post-translational modification state of class I HDACs.
المؤلفون: Hanigan TW; Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America., Taha TY; Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America., Aboukhatwa SM; Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America.; Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt., Frasor J; Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois, United States of America., Petukhov PA; Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
المصدر: PloS one [PLoS One] 2017 Oct 18; Vol. 12 (10), pp. e0186620. Date of Electronic Publication: 2017 Oct 18 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Histone Deacetylase Inhibitors/*pharmacology , Histone Deacetylases/*metabolism , Protein Processing, Post-Translational/*drug effects, Acetylation/drug effects ; Cytosol/drug effects ; Cytosol/enzymology ; Histone Deacetylase Inhibitors/chemistry ; Histones/metabolism ; Humans ; MCF-7 Cells ; Microscopy, Confocal ; Mitogens/pharmacology ; Models, Biological ; Phosphorylation/drug effects ; Protein Transport/drug effects ; Subcellular Fractions/drug effects ; Subcellular Fractions/enzymology
مستخلص: The mechanism of action of histone deacetylase inhibitors (HDACi) is mainly attributed to the inhibition of the deacetylase catalytic activity for their histone substrates. In this study, we analyzed the abundance of class I HDACs in the cytosolic, nuclear soluble and chromatin bound cellular fractions in breast cancer cells after HDACi treatment. We found that potent N-hydroxy propenamide-based HDACi induced a concentration dependent decrease in the HDAC1 associated with chromatin and a lasting concomitant increase in cytoplasmic HDAC1 while maintaining total protein expression. No such change occurred with HDAC2 or 8, however, an increase in cytoplasmic non-phosphorylated HDAC3 was also observed. The subcellular re-equilibration of HDAC1 was subsequent to the accumulation of acetylated histones and might be cell cycle dependent. This study suggests that the biological activity of a subset of N-hydroxy propenamide-based HDACi may stem from direct competition with histone substrates of HDACs as well as from spatial separation from their substrates in the nucleus and/or change in post-translational modification status of HDACs.
References: Nat Rev Drug Discov. 2014 Sep;13(9):673-91. (PMID: 25131830)
Structure. 2004 Jul;12(7):1325-34. (PMID: 15242608)
Int J Cancer. 2007 Sep 1;121(5):1138-48. (PMID: 17455259)
Nat Protoc. 2007;2(6):1445-57. (PMID: 17545981)
Cancer Res. 1983 Sep;43(9):3998-4006. (PMID: 6871841)
Mol Cell Biol. 2004 May;24(10 ):4546-56. (PMID: 15121871)
Tumour Biol. 2013 Feb;34(1):241-9. (PMID: 23055198)
FEBS Lett. 2000 Jul 28;478(1-2):77-83. (PMID: 10922473)
Cancer Res. 2003 Jul 1;63(13):3637-45. (PMID: 12839953)
Breast Cancer Res. 2015 Mar 07;17:33. (PMID: 25888415)
J Biol Chem. 2002 Jul 12;277(28):25748-55. (PMID: 11948178)
Biochem J. 2003 Mar 15;370(Pt 3):737-49. (PMID: 12429021)
Breast Cancer Res. 2012 May 21;14(3):R79. (PMID: 22613095)
J Biol Chem. 2006 Jan 27;281(4):2347-57. (PMID: 16293626)
Oncogene. 2005 Jul 7;24(29):4609-23. (PMID: 15897906)
Clin Cancer Res. 2006 Aug 1;12(15):4628-35. (PMID: 16899611)
J Clin Oncol. 2006 Jan 1;24(1):166-73. (PMID: 16330674)
Br J Cancer. 2012 Jan 3;106(1):77-84. (PMID: 22134508)
Eur J Clin Pharmacol. 2015 Jun;71(6):663-672. (PMID: 25939707)
J Biol Chem. 2004 Jun 11;279(24):25017-23. (PMID: 15082715)
J Cell Physiol. 2013 Jul;228(7):1525-35. (PMID: 23280436)
J Biol Chem. 2011 Jun 24;286(25):22211-8. (PMID: 21531716)
Cancer Lett. 2009 Aug 8;280(2):233-41. (PMID: 19344997)
J Biol Chem. 2002 May 31;277(22):19618-26. (PMID: 11919195)
Leukemia. 2008 May;22(5):1026-34. (PMID: 18256683)
Epigenomics. 2014 Feb;6(1):139-50. (PMID: 24579951)
J Biol Chem. 2013 Sep 13;288(37):26926-43. (PMID: 23897821)
Mol Pharm. 2013 Jan 7;10(1):337-52. (PMID: 23215027)
Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11700-5. (PMID: 12189205)
Am J Transl Res. 2012;4(1):24-43. (PMID: 22347520)
Int J Oncol. 2014 Mar;44(3):700-8. (PMID: 24366407)
Chem Biol. 2010 Jan 29;17(1):65-74. (PMID: 20142042)
Drug Metab Dispos. 2004 Oct;32(10):1132-8. (PMID: 15269190)
J Biol Chem. 2001 Oct 12;276(41):38307-19. (PMID: 11479283)
Biochem Biophys Res Commun. 1998 Apr 17;245(2):423-7. (PMID: 9571167)
Biochem J. 2000 Aug 15;350 Pt 1:199-205. (PMID: 10926844)
Proc Natl Acad Sci U S A. 2008 Mar 18;105(11):4179-84. (PMID: 18326024)
Cell Chem Biol. 2017 Nov 16;24(11):1356-1367.e8. (PMID: 28943357)
Nature. 2000 Nov 2;408(6808):106-11. (PMID: 11081517)
Mol Cancer Ther. 2003 Feb;2(2):151-63. (PMID: 12589032)
معلومات مُعتمدة: R01 CA131970 United States CA NCI NIH HHS; R01 HL130760 United States HL NHLBI NIH HHS; R21 CA183627 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Histone Deacetylase Inhibitors)
0 (Histones)
0 (Mitogens)
EC 3.5.1.98 (Histone Deacetylases)
تواريخ الأحداث: Date Created: 20171019 Date Completed: 20171030 Latest Revision: 20201214
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5646865
DOI: 10.1371/journal.pone.0186620
PMID: 29045501
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0186620