Transcriptome analysis of beta-catenin-related genes in CD34+ haematopoietic stem and progenitor cells from patients with AML Transcriptome analysis of beta-catenin-related genes in AML

Main Article Content

Buket Altinok Gunes
Tulin OZKAN
Aynur Karadag Gurel
Semih Dalkilic
Nevin Belder
Zeynep Ozkeserli
Hilal Ozdag Sevgili
Meral Beksac
Nilgun Sayinalp
Abdullah Munci Yagci
Asuman Sunguroglu

Keywords

AML, CD34+ cells, beta-catenin, microarray, DEGs

Abstract

Background: Acute myeloid leukaemia(AML) is a disease of the haematopoietic stem cells. Beta-catenin, a key element of the Wnt signalling, which is particularly active in various cancers. Our aim of this study was to determine beta-catenin gene expression levels in AML patients. Then, it is planned to compare the genes between AML grouped according to beta-catenin gene expression levels by DNA microarray. When the gene group identified in this way is combined with the genes in the control group, the aim is to determine the genes that are associated with beta-catenin in AML.


Methods: In this study, beta-catenin gene expression levels were determined in 19 AML patients and 3 controls by qRT-PCR. Transcriptome analysis was performed on AML grouped according to beta-catenin expression levels. Differentially expressed genes(DEGs) were identified and investigated with using DAVID, GO, KEGG and STRING.


Results: The transcriptome profiles of our AML samples showed different molecular signature profiles according on their beta-catenin levels(high-low). A total of 20 genes have been identified as hub genes. Among these, TTK, HJURP, KIF14 and BTF3, RPL17, RSL1D1 were found to be associated with poor survival and suggested to be associated with beta-catenin in AML. Furthermore, for the first time in our study, the ELOV6 gene, which is the most highly up-regulated gene in human AML samples, was correlated with a poor prognosis via beta-catenin high levels.


Conclusion: It is suggested that the identification of beta-catenin-related gene profiles in AML may help to select new therapeutic targets for the treatment of AML.

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