0441294 - BFÚ 2015 RIV US eng J - Journal Article
Steinmetz, B. - Hackl, H. - Slabáková, Eva - Schwarzinger, I. - Smějová, M. - Spittler, A. - Arbesu, I. - Shehata, M. - Souček, Karel - Wieser, R.
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Cell Cycle. Roč. 13, č. 18 (2014), s. 2931-2943. ISSN 1538-4101. E-ISSN 1551-4005
Institutional support: RVO:68081707
Keywords : apoptosis * cell cycle * EVI1
Subject RIV: BO - Biophysics
Impact factor: 4.565, year: 2014

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.
Permanent Link: http://hdl.handle.net/11104/0244359