دورية أكاديمية
أعرض في EDS

Lamin A/C Is Required for ChAT-Dependent Neuroblastoma Differentiation.

التفاصيل البيبلوغرافية
العنوان: Lamin A/C Is Required for ChAT-Dependent Neuroblastoma Differentiation.
المؤلفون: Guglielmi L; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy., Nardella M; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy., Musa C; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy., Iannetti I; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy., Arisi I; Genomics Facility, European Brain Research Institute (EBRI), Rome, Italy., D'Onofrio M; Genomics Facility, European Brain Research Institute (EBRI), Rome, Italy., Storti A; Genomics Facility, European Brain Research Institute (EBRI), Rome, Italy., Valentini A; Department of Laboratory Medicine and Department of Internal Medicine, PTV, University of Rome 'Tor Vergata', Rome, Italy., Cacci E; Department of Biology and Biotechnology 'Charles Darwin', Sapienza University, Rome, Italy., Biagioni S; Department of Biology and Biotechnology 'Charles Darwin', Sapienza University, Rome, Italy., Augusti-Tocco G; Department of Biology and Biotechnology 'Charles Darwin', Sapienza University, Rome, Italy., D'Agnano I; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy. igea.dagnano@cnr.it., Felsani A; CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy. armando.felsani@cnr.it.
المصدر: Molecular neurobiology [Mol Neurobiol] 2017 Jul; Vol. 54 (5), pp. 3729-3744. Date of Electronic Publication: 2016 May 25.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Humana Press Country of Publication: United States NLM ID: 8900963 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-1182 (Electronic) Linking ISSN: 08937648 NLM ISO Abbreviation: Mol Neurobiol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Clifton, NJ : Humana Press, c1987-
مواضيع طبية MeSH: Cell Differentiation*/drug effects , Cell Differentiation*/genetics, Choline O-Acetyltransferase/*metabolism , Lamin Type A/*metabolism , Neuroblastoma/*enzymology , Neuroblastoma/*pathology, Animals ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Knockdown Techniques ; Gene Ontology ; Mice ; Neuroblastoma/genetics ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Protein Interaction Mapping ; Receptors, Cholinergic/metabolism ; Receptors, Muscarinic/metabolism ; Transcription, Genetic/drug effects ; Tretinoin/pharmacology ; Up-Regulation/drug effects
مستخلص: The mouse neuroblastoma N18TG2 clone is unable to differentiate and is defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. The engagement of the 2/4 cells in the neuronal developmental program was confirmed by the increase of the expression level of several differentiation-related genes and by the reduction of the amount of transcripts of cell cycle genes. At the same time, we observed a massive reorganization of cytoskeletal proteins in terms of gene expression, with the accumulation of the nucleoskeletal lamina component Lamin A/C in differentiating cells. The increase of the Lmna transcripts induced by ChAT expression in 2/4 cells was mimicked treating the parental N18TG2 cells with the acetylcholine receptor agonist carbachol, thus demonstrating the direct role played by this receptor in neuron nuclei maturation. Conversely, a treatment of 2/4 cells with the muscarinic receptor antagonist atropine resulted in the reduction of the amount of Lmna RNA. Finally, the hypothesis that Lmna gene product might play a crucial role in the ChAT-dependent molecular differentiation cascade was strongly supported by Lmna knockdown in 2/4 cells leading to the downregulation of genes involved in differentiation and cytoskeleton formation and to the upregulation of genes known to regulate self-renewal and stemness.
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فهرسة مساهمة: Keywords: Choline acetyltransferase; Differentiation; Gene expression; LMNA; Neuroblastoma
المشرفين على المادة: 0 (Lamin Type A)
0 (Receptors, Cholinergic)
0 (Receptors, Muscarinic)
5688UTC01R (Tretinoin)
EC 2.3.1.6 (Choline O-Acetyltransferase)
تواريخ الأحداث: Date Created: 20160526 Date Completed: 20180309 Latest Revision: 20181113
رمز التحديث: 20221213
DOI: 10.1007/s12035-016-9902-6
PMID: 27221609
قاعدة البيانات: MEDLINE
الوصف
تدمد:1559-1182
DOI:10.1007/s12035-016-9902-6