Abstract:
:The ETS transcription factor ERG has been implicated as a major regulator of both normal and aberrant hematopoiesis. In acute myeloid leukemias harboring t(16;21), ERG function is deregulated due to a fusion with FUS/TLS resulting in the expression of a FUS-ERG oncofusion protein. How this oncofusion protein deregulates the normal ERG transcription program is unclear. Here, we show that FUS-ERG acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype. Moreover, in t(16;21) FUS-ERG co-occupies genomic regions bound by the nuclear receptor heterodimer RXR:RARA inhibiting target gene expression and interfering with hematopoietic differentiation. All-trans retinoic acid treatment of t(16;21) cells as well as FUS-ERG knockdown alleviate the myeloid-differentiation block. Together, the results suggest that FUS-ERG acts as a transcriptional repressor of the retinoic acid signaling pathway.
journal_name
Oncogenejournal_title
Oncogeneauthors
Sotoca AM,Prange KH,Reijnders B,Mandoli A,Nguyen LN,Stunnenberg HG,Martens JHdoi
10.1038/onc.2015.261subject
Has Abstractpub_date
2016-04-14 00:00:00pages
1965-76issue
15eissn
0950-9232issn
1476-5594pii
onc2015261journal_volume
35pub_type
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