Interleukin 6 signaling regulates promyelocytic leukemia protein gene expression in human normal and cancer cells
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F12%3A00390227" target="_blank" >RIV/68378050:_____/12:00390227 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1074/jbc.M111.316869" target="_blank" >http://dx.doi.org/10.1074/jbc.M111.316869</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1074/jbc.M111.316869" target="_blank" >10.1074/jbc.M111.316869</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Interleukin 6 signaling regulates promyelocytic leukemia protein gene expression in human normal and cancer cells
Popis výsledku v původním jazyce
Tumor suppressor PML is induced under viral and genotoxic stresses by interferons and JAK-STAT signaling. However, the mechanism responsible for its cell type-specific regulation under non-stimulated conditions is poorly understood. To analyze the variation of PML expression, we utilized three human cell types, BJ fibroblasts and HeLa and U2OS cell lines, each with a distinct PML expression pattern. Analysis of JAK-STAT signaling in the three cell lines revealed differences in levels of activated STAT3but not STAT1 correlating with PML mRNA and protein levels. RNAi-mediated knockdown of STAT3 decreased PML expression; both STAT3 level/activity and PML expression relied on IL6 secreted into culture media. We mapped the IL6-responsive sequence to an ISRE(-595/-628) element of the PML promoter. The PI3K/Akt/NF kappa B branch of IL6 signaling showed also cell-type dependence, being highest in BJ, intermediate in HeLa, and lowest in U2OS cells and correlated with IL6 secretion. RNAi-mediat
Název v anglickém jazyce
Interleukin 6 signaling regulates promyelocytic leukemia protein gene expression in human normal and cancer cells
Popis výsledku anglicky
Tumor suppressor PML is induced under viral and genotoxic stresses by interferons and JAK-STAT signaling. However, the mechanism responsible for its cell type-specific regulation under non-stimulated conditions is poorly understood. To analyze the variation of PML expression, we utilized three human cell types, BJ fibroblasts and HeLa and U2OS cell lines, each with a distinct PML expression pattern. Analysis of JAK-STAT signaling in the three cell lines revealed differences in levels of activated STAT3but not STAT1 correlating with PML mRNA and protein levels. RNAi-mediated knockdown of STAT3 decreased PML expression; both STAT3 level/activity and PML expression relied on IL6 secreted into culture media. We mapped the IL6-responsive sequence to an ISRE(-595/-628) element of the PML promoter. The PI3K/Akt/NF kappa B branch of IL6 signaling showed also cell-type dependence, being highest in BJ, intermediate in HeLa, and lowest in U2OS cells and correlated with IL6 secretion. RNAi-mediat
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
EB - Genetika a molekulární biologie
OECD FORD obor
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Návaznosti výsledku
Projekt
<a href="/cs/project/GA204%2F08%2F1418" target="_blank" >GA204/08/1418: Úloha signalizační dráhy JAK/STAT v buněčné senescenci</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2012
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Journal of Biological Chemistry
ISSN
0021-9258
e-ISSN
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Svazek periodika
287
Číslo periodika v rámci svazku
32
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
12
Strana od-do
26702-26714
Kód UT WoS článku
000307386000021
EID výsledku v databázi Scopus
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