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Evaluation of CCAAT/Enhancer Binding Protein (C/EBP) Alpha (CEBPA) and Runt‐Related Transcription Factor 1 (RUNX1) Expression in Patients with De Novo Acute Myeloid Leukemia
Author(s) -
Salarpour Fatemeh,
Goudarzipour Kourosh,
Mohammadi Mohammad Hossein,
Ahmadzadeh Ahmad,
Faraahi Sara,
Farsani Mehdi Allahbakhshian
Publication year - 2017
Publication title -
annals of human genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 77
eISSN - 1469-1809
pISSN - 0003-4800
DOI - 10.1111/ahg.12210
Subject(s) - cebpa , myeloid leukemia , runx1 , biology , transcription factor , myeloid , enhancer , myelopoiesis , cancer research , gene expression , gene , microbiology and biotechnology , genetics , haematopoiesis , stem cell
Summary The CCAAT/enhancer binding protein (C/EBP) alpha (CEBPA) and Runt‐related transcription factor 1 (RUNX1) genes have been traditionally regarded as two essential genes involved in normal myeloid maturation. Although the link between mutations in these genes and the development of acute myeloid leukemia (AML) has been extensively documented, the ramifications of gene expression dysregulations of CEBPA and RUNX1 has drawn less attention. The present study investigated CEBPA and RUNX1 gene expression levels in 96 primary AML specimens against a normal control group by way of real‐time RT‐PCR. Our results reveal that CEBPA and RUNX1 gene expression levels were unexpectedly and significantly higher in patients with AML when compared to the levels detected in the normal control group ( P < 0.0001). Furthermore, the correlation between CEBPA and RUNX1 was significant and positive ( P ‐value: 0.011, r : 0.257). Our data contradicts the widely established role of CEBPA and RUNX1 in myeloid differentiation, as we saw lower levels of CEBPA and RUNX1 expression to be exhibited in patients with AML. Likely, our data demonstrates that higher levels of CEBPA and RUNX1 expression were closely correlated with reduced myeloid maturation, but this idea needs to approved. It suggests that despite the current established functions of genes involved in cell differentiation, the leukemogenesis process has the capability to transform normal hematopoietic precursors in a manner that may employ the differentiation related gene at the service of malignancy.