Hypoxia-mediated histone acetylation and expression of N-myc transcription factor dictate aggressiveness of neuroblastoma cells
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F14%3A10282804" target="_blank" >RIV/00216208:11310/14:10282804 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/62156489:43210/14:00217640 RIV/00216208:11130/14:10282804 RIV/00216305:26620/14:PU112645 RIV/00064203:_____/14:10282804
Výsledek na webu
<a href="http://dx.doi.org/10.3892/or.2014.2999" target="_blank" >http://dx.doi.org/10.3892/or.2014.2999</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3892/or.2014.2999" target="_blank" >10.3892/or.2014.2999</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Hypoxia-mediated histone acetylation and expression of N-myc transcription factor dictate aggressiveness of neuroblastoma cells
Popis výsledku v původním jazyce
Cells of solid malignancies generally adapt to entire lack of oxygen. Hypoxia induces the expression of several genes, which allows the cells to survive. For DNA transcription, it is necessary that DNA structure is loosened. In addition to structural characteristics of DNA, its epigenetic alterations influence a proper DNA transcription. Since histones play a key role in epigenetics, changes in expression levels of acetylated histones H3 and H4 as well as of hypoxia-inducible factor-1 alpha (HIF-1 alpha) in human neuroblastoma cell lines cultivated under standard or hypoxic conditions (1% O-2) were investigated. Moreover, the effect of hypoxia on the expression of two transcription factors, c-Myc and N-myc, was studied. Hypoxic stress increased levelsof acetylated histones H3 and H4 in UKF-NB-3 and UKF-NB-4 neuroblastoma cells with N-myc amplification, whereas almost no changes in acetylation of these histones were found in an SK-N-AS neuroblastoma cell line, the line with diploid N-m
Název v anglickém jazyce
Hypoxia-mediated histone acetylation and expression of N-myc transcription factor dictate aggressiveness of neuroblastoma cells
Popis výsledku anglicky
Cells of solid malignancies generally adapt to entire lack of oxygen. Hypoxia induces the expression of several genes, which allows the cells to survive. For DNA transcription, it is necessary that DNA structure is loosened. In addition to structural characteristics of DNA, its epigenetic alterations influence a proper DNA transcription. Since histones play a key role in epigenetics, changes in expression levels of acetylated histones H3 and H4 as well as of hypoxia-inducible factor-1 alpha (HIF-1 alpha) in human neuroblastoma cell lines cultivated under standard or hypoxic conditions (1% O-2) were investigated. Moreover, the effect of hypoxia on the expression of two transcription factors, c-Myc and N-myc, was studied. Hypoxic stress increased levelsof acetylated histones H3 and H4 in UKF-NB-3 and UKF-NB-4 neuroblastoma cells with N-myc amplification, whereas almost no changes in acetylation of these histones were found in an SK-N-AS neuroblastoma cell line, the line with diploid N-m
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
CE - Biochemie
OECD FORD obor
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Návaznosti výsledku
Projekt
<a href="/cs/project/GAP301%2F10%2F0356" target="_blank" >GAP301/10/0356: Studie participace specifických mechanismů poškození DNA na cytoxicitě cytostatik vůči lidským chemosensitivním a chemorestentním neuroblastomům</a><br>
Návaznosti
S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2014
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Oncology Reports
ISSN
1021-335X
e-ISSN
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Svazek periodika
31
Číslo periodika v rámci svazku
4
Stát vydavatele periodika
GR - Řecká republika
Počet stran výsledku
7
Strana od-do
1928-1934
Kód UT WoS článku
000334345600057
EID výsledku v databázi Scopus
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