Abstract
Prognostic molecular markers identified in leukemia are becoming increasingly important especially in risk stratification and to determine therapy. In this study, we investigate the role of ELK-1 transcription factor and its potential target genes in four cell lines; Daudi, Jurkat, K-562 and HL-60. To evaluate ELK-1, MCPIP, MCL-1, BCL-10, CEBPB and SRF genes expression profiles we have performed a Real-time PCR analysis on Daudi, Jurkat, K-562 and HL-60 cell lines. ELK-1 over expression concomitant with SRF overexpression was detected only in Daudi cell line while only SRF overexpression was detected in jurkat cells. Expression of MCPIP, MCL-1, BCL-10 and CEBPB genes were decreased in all cell lines. Protein levels or phosphorylation status of ELK-1, BCL-10, CEBPB, MCL-1, MCPIP and SRF, moreover, changes that may occur when ELK-1 continuous overexpression is provided or completely silenced in these cell lines have not been evaluated. These questions are suggestions for future investigations.
Highlights
Understanding the pathogenesis of and identification markers to diagnose leukemia is still the subject of many studies
ELK-1, MCPIP, Myeloid Cell Leukemia 1 (MCL-1), B cell CLL/lymphoma 10 (BCL-10), CEBPB and serum response factor (SRF) genes expression were determined in Human leukemia cell lines Jurkat, K-562, HL-60 and lymphoma cell line Daudi
Glyceraldehyde Phosphate Dehydrogenase (GAPDH) was used as endogenous control and Control group accepted as reference sample
Summary
Understanding the pathogenesis of and identification markers to diagnose leukemia is still the subject of many studies. Recurrent balanced structural rearrangements are very important in diagnosis and accepted as prognostic factors in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL) and other hematologic malignancies [1]. Some imbalanced chromosomal abnormalities, especially submicroscopic rearrangements, cannot be detected by conventional cytogenetics [2]. We have used oligo array Comparative Genomic Hybridization (oaCGH) to characterize chromosomal rearrangements in 41 acute leukemia samples. One of the prominent one was the recurrent duplication of the ELK-1 oncogene which was observed in both ALL and AML cases. We have reported deletion of CEBPB (CCAAT Enhancer Binding Protein-B) and duplication of serum response factor (SRF) in AML patients [3]
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