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| Home > Publications database > p19-INK4d inhibits neuroblastoma cell growth, induces differentiation and is hypermethylated and downregulated in MYCN-amplified neuroblastomas. > print |
| Home > Publications database > p19-INK4d inhibits neuroblastoma cell growth, induces differentiation and is hypermethylated and downregulated in MYCN-amplified neuroblastomas. > print |
| 001 | 119889 | ||
| 005 | 20240228134958.0 | ||
| 024 | 7 | _ | |a 10.1093/hmg/ddu406 |2 doi |
| 024 | 7 | _ | |a pmid:25104850 |2 pmid |
| 024 | 7 | _ | |a 0964-6906 |2 ISSN |
| 024 | 7 | _ | |a 1460-2083 |2 ISSN |
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| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 570 |
| 100 | 1 | _ | |a Dreidax, Daniel |0 P:(DE-He78)00d281bd33b8c1254cbe4f048dbfaa14 |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a p19-INK4d inhibits neuroblastoma cell growth, induces differentiation and is hypermethylated and downregulated in MYCN-amplified neuroblastomas. |
| 260 | _ | _ | |a Oxford |c 2014 |b Oxford Univ. Press |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1490257136_30632 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Uncontrolled 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. |
| 536 | _ | _ | |a 312 - Functional and structural genomics (POF3-312) |0 G:(DE-HGF)POF3-312 |c POF3-312 |f POF III |x 0 |
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| 650 | _ | 7 | |a Antimetabolites, Antineoplastic |2 NLM Chemicals |
| 650 | _ | 7 | |a CDKN2D protein, human |2 NLM Chemicals |
| 650 | _ | 7 | |a Cyclin-Dependent Kinase Inhibitor p19 |2 NLM Chemicals |
| 650 | _ | 7 | |a MYCN protein, human |2 NLM Chemicals |
| 650 | _ | 7 | |a N-Myc Proto-Oncogene Protein |2 NLM Chemicals |
| 650 | _ | 7 | |a Nuclear Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Oncogene Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Tretinoin |0 5688UTC01R |2 NLM Chemicals |
| 650 | _ | 7 | |a decitabine |0 776B62CQ27 |2 NLM Chemicals |
| 650 | _ | 7 | |a Azacitidine |0 M801H13NRU |2 NLM Chemicals |
| 700 | 1 | _ | |a Bannert, Steffen |0 P:(DE-He78)df0b5bf4e9b9232224948f0d0ff87210 |b 1 |u dkfz |
| 700 | 1 | _ | |a Henrich, Kai-Oliver |0 P:(DE-He78)a579ca2567736066534409e732b31c91 |b 2 |u dkfz |
| 700 | 1 | _ | |a Schröder, Christina |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Bender, Sebastian |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Oakes, Christopher C |0 P:(DE-HGF)0 |b 5 |
| 700 | 1 | _ | |a Lindner, Sven |b 6 |
| 700 | 1 | _ | |a Schulte, Johannes H |b 7 |
| 700 | 1 | _ | |a Duffy, David |b 8 |
| 700 | 1 | _ | |a Schwarzl, Thomas |b 9 |
| 700 | 1 | _ | |a Saadati, Maral |0 P:(DE-He78)609d3f1c1420bf59b2332eeab889cb74 |b 10 |u dkfz |
| 700 | 1 | _ | |a Ehemann, Volker |b 11 |
| 700 | 1 | _ | |a Benner, Axel |0 P:(DE-He78)e15dfa1260625c69d6690a197392a994 |b 12 |u dkfz |
| 700 | 1 | _ | |a Pfister, Stefan |0 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9 |b 13 |u dkfz |
| 700 | 1 | _ | |a Fischer, Matthias |b 14 |
| 700 | 1 | _ | |a Westermann, Frank |0 P:(DE-He78)91f32735ee876c579d63c05a7f4778dd |b 15 |e Last author |u dkfz |
| 773 | _ | _ | |a 10.1093/hmg/ddu406 |g Vol. 23, no. 25, p. 6826 - 6837 |0 PERI:(DE-600)1474816-2 |n 25 |p 6826 - 6837 |t Human molecular genetics |v 23 |y 2014 |x 1460-2083 |
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