Tehran University of Medical Sciences International Journal of Hematology-Oncology and Stem Cell Research 2008-2207 14 1 2020 01 01 72 92 EN Mat Jusoh Siti Asmaa Department of Hematology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia Hamid Ali Al-Jamal Diagnostic and Biomedicine, Faculty of Health Sciences, Universiti Sultan Zainal Abidin, Gong Badak Campus, Kuala Nerus, 21300, Terengganu, Malaysia Abdul Rahim Hussein Regenerative Medicine Cluster, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Pulau Pinang, Malaysia Badrul Hisham Yahaya Regenerative Medicine Cluster, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Pulau Pinang, Malaysia Azlan Husin Department of Internal Medicine, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia Rosline Hassan Department of Hematology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia Faezahtul Arbaeyah Hussain Department of Pathology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia Shaharum Shamsuddin School of Health Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia. AND Institute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia Muhammad Farid Johan Department of Hematology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia 2019 02 14 2019 04 27 Background: Acute myeloid leukemia (AML) is the most common form of acute leukemias in adults which is clinically and molecularly heterogeneous. Several risk and genetic factors have been widely investigated to characterize AML. However, the concomitant epigenetic factors in controlling the gene expression lead to AML transformation was not fully understood. This study was aimed to identify epigenetically regulated genes in AML cell lines induced by epigenetic modulating agents, Trichostatin A (TSA) and 5-Azacytidine (5-Aza). Methods: MV4-11 and Kasumi 1 were treated with TSA and/or 5-Aza at IC50concentration. Gene expression profiling by microarray was utilized using SurePrint G3 Human Gene Expression v3. Gene ontology and KEGG pathway annotations were analyzed by DAVID bioinformatics software using EASE enrichment score. mRNA expression of the differentially expressed genes were verified by quantitative real time PCR. Results: Gene expression analysis revealed a significantchanges in the expression of 24,822, 15,720, 15,654 genes in MV4-11 and 12,598, 8828, 18,026 genes in Kasumi 1, in response to TSA, 5-Aza and combination treatments, respectively, compared to non-treated (p<0.05). 7 genes (SOCS3,TUBA1C, CCNA1, MAP3K6, PTPRC, STAT6and RUNX1) and 4 genes (ANGPTL4, TUBB2A, ADAM12and PTPN6) shown to be predominantly expressed in MV4-11 and Kasumi 1, respectively (EASE<0.1). The analysis also revealed phagosome pathway commonly activated in both cell lines. Conclusion: Our data showed a distinct optimal biological characteristic and pathway in different types of leukemic cell lines. These finding may help in the identification of cell-specific epigenetic biomarker in the pathogenesis of AML. https://ijhoscr.tums.ac.ir/index.php/ijhoscr/article/view/1084 https://ijhoscr.tums.ac.ir/index.php/ijhoscr/article/download/1084/825