The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F14%3A00107098" target="_blank" >RIV/00216224:14310/14:00107098 - isvavai.cz</a>

Alternative codes found

RIV/68081707:_____/14:00441294 RIV/00159816:_____/14:00061230

Result on the web

<a href="https://www.tandfonline.com/doi/pdf/10.4161/15384101.2014.946869?needAccess=true" target="_blank" >https://www.tandfonline.com/doi/pdf/10.4161/15384101.2014.946869?needAccess=true</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4161/15384101.2014.946869" target="_blank" >10.4161/15384101.2014.946869</a>

Result language

angličtina

Original language name

The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid

Original language description

The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RAR gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well as biological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF- superfamily of cytokines. In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects. The potential clinical implications of these findings are discussed.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10601 - Cell biology

Project

—

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2014

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Cell Cycle

ISSN

1538-4101

e-ISSN

1551-4005

Volume of the periodical

13

Issue of the periodical within the volume

18

Country of publishing house

US - UNITED STATES

Number of pages

13

Pages from-to

2931-2943

UT code for WoS article

000348325800020

EID of the result in the Scopus database

2-s2.0-84908158155