Inhibition of the cell death pathway in non-alcoholic ...€¦ · global and gene-specific deacetylation of histone H4 lysine 16 (H4K16). Pathway analysis of the entire set of differentially
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Inhibition of the cell death pathway in non-alcoholic steatohepatitis (NASH)-related hepatocarcinogenesis is associated with histone H4 lysine 16 deacetylation
Aline de Conti1,*, Kostiantyn Dreval1,*, Volodymyr Tryndyak1, Orish E. Orisakwe1,2, Sharon A.
Ross3, Frederick A. Beland1, and Igor P. Pogribny1,§
1Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson,
Arkansas 72079, USA 2Department of Experimental Pharmacology and Toxicology, University of Port-Harcourt, Rivers
State, Nigeria
3Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland 20892, USA
* Aline de Conti and Kostiantyn Dreval contributed equally to this article.
Running title: Cell death inhibition in NASH-related hepatocarcinogenesis.
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
5. White DL, Kanwal F, El-Serag HB. Association between nonalcoholic fatty liver disease and risk for hepatocellular cancer, based on systematic review. Clin Gastroenterol Hepatol 2012;10:1342-59.
6. Younossi ZM, Otgonsuren M, Henry L, Venkatesan C, Mishra A, Erario M, et al. Association of nonalcoholic fatty liver disease (NAFLD) with hepatocellular carcinoma (HCC) in the United States from 2004 to 2009. Hepatology 2015;62:1723-30.
7. Cohen JC, Horton JD, Hobbs HH. Human fatty liver disease: old questions and new insights. Science 2011;332:1519-23.
8. Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease–meta‐analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016;64:73-84.
9. Zucman-Rossi J, Villanueva A, Nault J-C, Llovet JM. Genetic landscape and biomarkers of hepatocellular carcinoma. Gastroenterology 2015;149:1226-39.
10. Pogribny IP, Rusyn I. Role of epigenetic aberrations in the development and progression of human hepatocellular carcinoma. Cancer Lett 2014;342:223-30.
11. Fujii M, Shibazaki Y, Wakamatsu K, Honda Y, Kawauchi Y, Suzuki K, et al. A murine model for non-alcoholic steatohepatitis showing evidence of association between diabetes and hepatocellular carcinoma. Med Mol Morphol 2013;46:141-52.
12. Takakura K, Koido S, Fujii M, Hashiguchi T, Shibazaki Y, Yoneyama H, et al. Characterization of non-alcoholic steatohepatitis-derived hepatocellular carcinoma as a human stratification model in mice. Anticancer Res 2014;34:4849-55.
13. Machado MV, Michelotti GA, Xie G, de Almeida PT, Boursier J, Bohnic B, et al. Mouse models of diet-induced nonalcoholic steatohepatitis reproduce the heterogeneity of the human disease. PLoS One 2015;10:e01323
14. Fang H, Harris SC, Su Z, Chen M, Qian F, Shi L, et al. ArrayTrack: an FDA and public genomic tool. Methods Mol Biol 2009;563:379-98.
15. Benjamini Y, Hochberg Y. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J R Stat Soc Series B Stat Methodol 1995;57:289-300.
16. Krämer A, Green J, Pollard J Jr, Tugendreich S. Causal analysis approaches in Ingenuity Pathway Analysis. Bioinformatics 2014;30:523-30.
17. Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative CT method. Nat Protoc 2008;3:1101-8.
18. de Conti A, Kobets T, Escudero-Lourdes C, Montgomery B, Tryndyak V, Beland FA, et al. Dose- and time-dependent epigenetic changes in the livers of Fisher 344 rats exposed to furan. Toxicol Sci 2014;139:371-80.
19. Schattenberg JM, Schuchmann M, Galle PR. Cell death and hepatocarcinogenesis: dysregulation of apoptosis signaling pathways. J Gastroenterol Hepatol 2011;26 (Suppl 1):213-9.
20. Liedtke C, Trautwein C. The role of TNF and Fas dependent signaling in animal models of inflammatory liver injury and liver cancer. Eur J Cell Biol 2012;91:582-9.
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
21. Brenner C, Galluzzi L, Kepp O, Kroemer G. Decoding cell death signals in liver inflammation. J Hepatol 2013;59:583-94.
22. Waetzig GH, Rosenstiel P, Arlt A, Till A, Bräutigam K, Schäfer H, et al. Soluble tumor necrosis factor (TNF) receptor-1 induces apoptosis via reverse TNF signaling and autocrine transforming growth factor-β1. FASEB J 2005; 19:91-3.
23. Lakshman M, Subramaniam V, Wong S, Jothy S. CD44 promotes resistance to apoptosis in murine colonic epithelium. J Cell Physiol 2005;203:583-588.
24. Fernando J, Malfettone A, Cepeda EB, Vilarrasa‐Blasi R, Bertran E, Raimondi G, et al. A mesenchymal‐like phenotype and expression of CD44 predict lack of apoptotic response to sorafenib in liver tumor cells. Int J Cancer 2015;136: E161- E172.
25. Olsson M, Zhivotovsky B. Caspases and cancer. Cell Death Differ 2011;18:1441-1449. 26. Green DR, Llambi F. Cell death signaling. Cold Spring Harb Perspect Biol
2015;7:a006080. 27. Chi P, Allis CD, Wang GG. Covalent histone modifications – miswritten, misinterpreted
and mis-erased in human cancers. Nat Rev Cancer 2010;10:457-69. 28. Gry M, Rimini R, Strömberg S, Asplund A, Pontén F, Uhlén M, et al. Correlations
between RNA and protein expression profiles in 23 human cell lines. BMC Genomics 2009;10:365.
29. Schotta G, Lachner M, Sarma K, Ebert A, Sengupta R, Reuter G, et al. A silencing pathway to induce H3-K9 and H4-K20 trimethylation at constitutive heterochromatin. Genes Dev 2004;18:1251-62.
30. Taipale M, Rea S, Richter K, Vilar A, Lichter P, Imhof A, et al. hMOF histone acetyltransferase is required for histone H4 lysine 16 acetylation in mammalian cells. Mol Cell Biol 2005;25:6798-810.
31. Vaquero A, Sternglanz R, Reinberg D. NAD+-dependent deacetylation of H4 lysine 16 by class III HDACs. Oncogene 2007;26:5505-20.
32. Gironella M, Malicet C, Cano C, Sandi MJ, Hamidi T, Tauil RMN, et al. p8/nupr1 regulates DNA‐repair activity after double‐strand gamma irradiation‐induced DNA damage. J Cell Physiol 2009;221:594-602.
33. Aguado-Llera D, Hamidi T, Doménech R, Pantoja-Uceda D, Gironella M, Santoro J, et al. Deciphering the binding between Nupr1 and MSL1 and their DNA-repairing activity. PloS One 2013;8:e78101.
34. Chen D, Kluz T, Fang L, Zhang X, Sun H, Jin C, et al. Hexavalent chromium (Cr(VI)) down-regulates acetylation of histone H4 at lysine 16 through induction of stressor protein Nupr1. PloS One 2016;11:e0157317.
35. Fraga MF, Ballestar E, Villar-Garea A, Boix-Chornet M, Espada J, Schotta G, et al. Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer. Nat Genet 2005;37:391-400.
36. Baylin S, Bestor TH. Altered methylation patterns in cancer cell genomes: cause or consequence? Cancer Cell 2002;1:299-305.
37. Pitot HC. Hepatocyte death in hepatocarcinogenesis. Hepatology 1998;28:1-5.
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
38. Kikuchi S, Griffin CT, Wang S-S, Bissell DM. Role of CD44 in epithelial wound repair: migration of rat hepatic stellate cells utilizes hyaluronic acid and CD44v6. J Biol Chem 2005;280:15398-404.
39. Yovchev MI, Grozdanov PN, Zhou H, Racherla H, Guha C, Dabeva MD. Identification of adult hepatic progenitor cells capable of repopulating injured rat liver. Hepatology 2008;47:636-47.
40. Taylor GCA, Eskeland R, Hekimoglu-Balkan B, Pradeepa MM, Bickmore WA. H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction. Genome Res 2013;23:2053-65.
41. Wang R-H, Zhao T, Cui K, Hu G, Chen Q, Chen W, et al. Negative reciprocal regulation between Sirt1 and Per2 modulates the circadian clock and aging. Sci Rep 2016;6:28633.
42. Füllgrabe J, Lynch-Day MA, Heldring N, Li W, Struijk RB, Ma Q, et al. The histone H4 lysine 16 acetyltransferase hMOF regulates the outcome of autophagy. Nature 2013;500:468-71.
43. Cano CE, Hamidi T, Sandi MJ, Iovanna JL. Nupr1: the Swiss‐knife of cancer. J Cell Physiol 2011;226:1439-43.
44. Lee Y-K, Jee BA, Kwon SM, Yoon Y-S, Xu WG, Wang H-J, et al. Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression. Hepatology 2015;62:1174-89.
45. Bak Y, Shin H-j, Bak Is, Yoon D-y, Yu D-Y. Hepatitis B virus X promotes hepatocellular carcinoma development via nuclear protein 1 pathway. Biochem Biophys Res Commun 2015;466:676-81.
46. Emma MR, Iovanna JL, Bachvarov D, Puleio R, Loria GR, Augello G, et al. NUPR1, a new target in liver cancer: implication in controlling cell growth, migration, invasion and sorafenib resistance. Cell Death Dis 2016;7:e2269.
47. Sykes SM, Mellert HS, Holbert MA, Li K, Marmorstein R, Lane WS, et al. Acetylation of the p53 DNA-binding domain regulates apoptosis induction. Mol Cell 2006;24:841-51.
48. Pfister S, Rea S, Taipale M, Mendrzyk F, Straub B, Ittrich C, et al. The histone acetyltransferase hMOF is frequently downregulated in primary breast carcinoma and medulloblastoma and constitutes a biomarker for clinical outcome in medulloblastoma. Int J Cancer 2008;122:1207-13.
49. Cao L, Zhu L, Yang J, Su J, Ni J, Du Y, et al. Correlation of low expression of hMOF with clinicopathological features of colorectal carcinoma, gastric cancer and renal cell carcinoma. Int J Oncol 2014;44:1207-14.
50. Zhang J, Liu H, Pan H, Yang Y, Huang G, Yang Y, et al. The histone acetyltransferase hMOF suppresses hepatocellular carcinoma growth. Biochem Biophys Res Commun 2014;452:575-80.
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109
Published OnlineFirst May 16, 2017.Mol Cancer Res Aline de Conti, Kostiantyn Dreval, Volodymyr Tryndyak, et al. associated with histone H4 lysine 16 deacetylationsteatohepatitis (NASH)-related hepatocarcinogenesis is Inhibition of the cell death pathway in non-alcoholic
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Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on May 16, 2017; DOI: 10.1158/1541-7786.MCR-17-0109