Premium
Identification of transcripts modulated by ETV6 expression
Author(s) -
Boily Gino,
Larose Josiane,
Langlois Sylvie,
Sinnett Daniel
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2006.06377.x
Subject(s) - etv6 , gene , biology , transcription factor , gene expression , real time polymerase chain reaction , genetics , reverse transcription polymerase chain reaction , polymerase chain reaction , regulation of gene expression , cancer research , microbiology and biotechnology , chromosomal translocation
Summary Deletions at chromosome 12p12‐13 are observed in 26–47% of childhood pre‐B acute lymphoblastic leukaemia (ALL) cases, suggesting the presence of a tumour suppressor gene (TSG). Accumulating genetic and functional evidence points to ETV6 as being the most probable TSG targeted by the deletions. ETV6 is a ubiquitously expressed transcription factor of the ETS family with very few known targets. To understand its function and to elucidate the impact of its absence in leukaemia, we conducted a study to identify targeted genes. Following the induction of ETV6 expression, global expression was evaluated at different time points. We identified 87 modulated genes, of which 10 ( AKR1C1 , AKR1C3 , IL18 , LUM , PHLDA1 , PTGER4 , PTGS2 , SPHK1 , TP53 and VEGF ) were validated by real‐time quantitative reverse transcription‐polymerase chain reaction. To assess the significance of the validated candidate genes in leukaemia, their expression patterns were determined, as well as that of ETV6 , in pre‐B ALL patients. The expression of IL18 , LUM , PTGER4 , SPHK1 and TP53 was significantly correlated with that of ETV6, further suggesting that ETV6 could regulate the expression of these genes in leukaemia. This work constitutes another step towards the understanding of the functions of ETV6 and the impact of its inactivation in childhood leukaemia.