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000119889 1001_ $$0P:(DE-He78)00d281bd33b8c1254cbe4f048dbfaa14$$aDreidax, Daniel$$b0$$eFirst author$$udkfz
000119889 245__ $$ap19-INK4d inhibits neuroblastoma cell growth, induces differentiation and is hypermethylated and downregulated in MYCN-amplified neuroblastomas.
000119889 260__ $$aOxford$$bOxford Univ. Press$$c2014
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000119889 520__ $$aUncontrolled cell cycle entry, resulting from deregulated CDK-RB1-E2F pathway activity, is a crucial determinant of neuroblastoma cell malignancy. Here we identify neuroblastoma-suppressive functions of the p19-INK4d CDK inhibitor and uncover mechanisms of its repression in high-risk neuroblastomas. Reduced p19-INK4d expression was associated with poor event-free and overall survival and neuroblastoma risk factors including amplified MYCN in a set of 478 primary neuroblastomas. High MYCN expression repressed p19-INK4d mRNA and protein levels in different neuroblastoma cell models with conditional MYCN expression. MassARRAY and 450K methylation analyses of 105 primary neuroblastomas uncovered a differentially methylated region within p19-INK4d. Hypermethylation of this region was associated with reduced p19-INK4d expression. In accordance, p19-INK4d expression was activated upon treatment with the demethylating agent, 2'-deoxy-5-azacytidine, in neuroblastoma cell lines. Ectopic p19-INK4d expression decreased viability, clonogenicity and the capacity for anchorage-independent growth of neuroblastoma cells, and shifted the cell cycle towards the G1/0 phase. p19-INK4d also induced neurite-like processes and markers of neuronal differentiation. Moreover, neuroblastoma cell differentiation, induced by all-trans retinoic acid or NGF-NTRK1-signaling, activated p19-INK4d expression. Our findings pinpoint p19-INK4d as a neuroblastoma suppressor and provide evidence for MYCN-mediated repression and for epigenetic silencing of p19-INK4d by DNA hypermethylation in high-risk neuroblastomas.
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000119889 650_7 $$2NLM Chemicals$$aAntimetabolites, Antineoplastic
000119889 650_7 $$2NLM Chemicals$$aCDKN2D protein, human
000119889 650_7 $$2NLM Chemicals$$aCyclin-Dependent Kinase Inhibitor p19
000119889 650_7 $$2NLM Chemicals$$aMYCN protein, human
000119889 650_7 $$2NLM Chemicals$$aN-Myc Proto-Oncogene Protein
000119889 650_7 $$2NLM Chemicals$$aNuclear Proteins
000119889 650_7 $$2NLM Chemicals$$aOncogene Proteins
000119889 650_7 $$05688UTC01R$$2NLM Chemicals$$aTretinoin
000119889 650_7 $$0776B62CQ27$$2NLM Chemicals$$adecitabine
000119889 650_7 $$0M801H13NRU$$2NLM Chemicals$$aAzacitidine
000119889 7001_ $$0P:(DE-He78)df0b5bf4e9b9232224948f0d0ff87210$$aBannert, Steffen$$b1$$udkfz
000119889 7001_ $$0P:(DE-He78)a579ca2567736066534409e732b31c91$$aHenrich, Kai-Oliver$$b2$$udkfz
000119889 7001_ $$0P:(DE-HGF)0$$aSchröder, Christina$$b3
000119889 7001_ $$0P:(DE-HGF)0$$aBender, Sebastian$$b4
000119889 7001_ $$0P:(DE-HGF)0$$aOakes, Christopher C$$b5
000119889 7001_ $$aLindner, Sven$$b6
000119889 7001_ $$aSchulte, Johannes H$$b7
000119889 7001_ $$aDuffy, David$$b8
000119889 7001_ $$aSchwarzl, Thomas$$b9
000119889 7001_ $$0P:(DE-He78)609d3f1c1420bf59b2332eeab889cb74$$aSaadati, Maral$$b10$$udkfz
000119889 7001_ $$aEhemann, Volker$$b11
000119889 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b12$$udkfz
000119889 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b13$$udkfz
000119889 7001_ $$aFischer, Matthias$$b14
000119889 7001_ $$0P:(DE-He78)91f32735ee876c579d63c05a7f4778dd$$aWestermann, Frank$$b15$$eLast author$$udkfz
000119889 773__ $$0PERI:(DE-600)1474816-2$$a10.1093/hmg/ddu406$$gVol. 23, no. 25, p. 6826 - 6837$$n25$$p6826 - 6837$$tHuman molecular genetics$$v23$$x1460-2083$$y2014
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