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Background: The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.

Methods: Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.

Results: Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed in vitro, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.

Conclusion: The RelA/p65 inhibitory effects of SAHA and VPA in vitro and the close relationship of class I HDACs and RelA/p65 in vivo suggest that treatment with HDIs could serve as a promising approach to suppress NF-kappaB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.

Titel:	High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer in vitro and in vivo.
Autor/in / Beteiligte Person:	Lehmann, A ; Denkert, C ; Budczies, J ; Buckendahl, AC ; Darb-Esfahani, S ; Noske, A ; Müller, BM ; Bahra, M ; Neuhaus, P ; Dietel, M ; Kristiansen, G ; Weichert, W
Link:	Zum Volltext
Zeitschrift:	BMC cancer, Jg. 9 (2009-11-13), S. 395
Veröffentlichung:	London : BioMed Central, [2001-, 2009
Medientyp:	academicJournal
ISSN:	1471-2407 (electronic)
DOI:	10.1186/1471-2407-9-395
Schlagwort:	Adenocarcinoma enzymology Adenocarcinoma genetics Adenocarcinoma pathology Adult Aged Aged, 80 and over Cell Line, Tumor Cell Nucleus genetics Cell Nucleus metabolism Enzyme Inhibitors pharmacology Female Histone Deacetylase 1 genetics Histone Deacetylase 2 genetics Histone Deacetylases genetics Humans Male Middle Aged Pancreatic Neoplasms enzymology Pancreatic Neoplasms genetics Pancreatic Neoplasms pathology Transcription Factor RelA genetics Adenocarcinoma metabolism Gene Expression drug effects Histone Deacetylase 1 metabolism Histone Deacetylase 2 metabolism Histone Deacetylases metabolism Pancreatic Neoplasms metabolism Transcription Factor RelA metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [BMC Cancer] 2009 Nov 13; Vol. 9, pp. 395. <i>Date of Electronic Publication: </i>2009 Nov 13. MeSH Terms: Gene Expression* / drug effects ; Adenocarcinoma / metabolism ; Histone Deacetylase 1 / metabolism ; Histone Deacetylase 2 / metabolism ; Histone Deacetylases / metabolism ; Pancreatic Neoplasms / metabolism ; Transcription Factor RelA / metabolism ; Adenocarcinoma / enzymology ; Adenocarcinoma / genetics ; Adenocarcinoma / pathology ; Adult ; Aged ; Aged, 80 and over ; Cell Line, Tumor ; Cell Nucleus / genetics ; Cell Nucleus / metabolism ; Enzyme Inhibitors / pharmacology ; Female ; Histone Deacetylase 1 / genetics ; Histone Deacetylase 2 / genetics ; Histone Deacetylases / genetics ; Humans ; Male ; Middle Aged ; Pancreatic Neoplasms / enzymology ; Pancreatic Neoplasms / genetics ; Pancreatic Neoplasms / pathology ; Transcription Factor RelA / genetics References: Nat Rev Genet. 2002 Jun;3(6):415-28. (PMID: 12042769) ; Cell Mol Life Sci. 2001 May;58(5-6):728-36. (PMID: 11437234) ; Nat Rev Cancer. 2001 Dec;1(3):194-202. (PMID: 11902574) ; Oncogene. 2002 Sep 19;21(42):6510-9. (PMID: 12226754) ; Rev Recent Clin Trials. 2007 Jan;2(1):69-75. (PMID: 18473990) ; Annu Rev Immunol. 1998;16:225-60. (PMID: 9597130) ; Curr Med Chem. 2003 Nov;10(22):2351-8. (PMID: 14529478) ; Ann Surg. 2004 Jun;239(6):763-9; discussion 769-71. (PMID: 15166955) ; Cell Death Differ. 2005 Apr;12(4):395-404. (PMID: 15665816) ; Nat Rev Cancer. 2006 Jan;6(1):38-51. (PMID: 16397526) ; Clin Cancer Res. 2008 Mar 15;14(6):1669-77. (PMID: 18347167) ; Br J Cancer. 2007 Aug 20;97(4):523-30. (PMID: 17622249) ; Cell. 2002 Feb 22;108(4):489-500. (PMID: 11909520) ; Cancer Res. 2006 May 15;66(10):5409-18. (PMID: 16707469) ; Nat Rev Drug Discov. 2006 Sep;5(9):769-84. (PMID: 16955068) ; Biochem J. 2003 Mar 15;370(Pt 3):737-49. (PMID: 12429021) ; J Biol Chem. 2006 Mar 3;281(9):5612-22. (PMID: 16377638) ; Expert Opin Investig Drugs. 2007 Jul;16(7):1111-20. (PMID: 17594194) ; Mol Cancer Res. 2005 Feb;3(2):100-9. (PMID: 15755876) ; J Pathol. 2000 Jun;191(2):154-61. (PMID: 10861575) ; Br J Cancer. 2008 Feb 12;98(3):604-10. (PMID: 18212746) ; Science. 2001 Aug 31;293(5535):1653-7. (PMID: 11533489) ; J Med Chem. 2003 Nov 20;46(24):5097-116. (PMID: 14613312) ; Lancet Oncol. 2008 Feb;9(2):139-48. (PMID: 18207460) ; Nat Rev Cancer. 2002 Apr;2(4):301-10. (PMID: 12001991) ; Nat Biotechnol. 2007 Jan;25(1):84-90. (PMID: 17211407) ; EMBO J. 2001 Dec 17;20(24):6969-78. (PMID: 11742974) ; Cancer Res. 2004 Feb 15;64(4):1331-7. (PMID: 14973050) ; Oncogene. 2003 May 22;22(21):3243-51. (PMID: 12761494) ; Oncogene. 2007 Aug 13;26(37):5541-52. (PMID: 17694093) ; CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66. (PMID: 17237035) ; Pancreas. 2008 Apr;36(3):e1-9. (PMID: 18362831) ; J Biol Chem. 2006 May 12;281(19):13548-13558. (PMID: 16533812) Substance Nomenclature: 0 (Enzyme Inhibitors) ; 0 (Transcription Factor RelA) ; EC 3.5.1.98 (HDAC1 protein, human) ; EC 3.5.1.98 (HDAC2 protein, human) ; EC 3.5.1.98 (Histone Deacetylase 1) ; EC 3.5.1.98 (Histone Deacetylase 2) ; EC 3.5.1.98 (Histone Deacetylases) ; EC 3.5.1.98 (histone deacetylase 3) Entry Date(s): Date Created: 20091117 Date Completed: 20100113 Latest Revision: 20211020 Update Code: 20240513 PubMed Central ID: PMC2779818

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High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer in vitro and in vivo.