Abstract

Lamiaa A. Mohamed*, Magdy M. Mohamed, Marwa G. A. Hegazy and Nashwa El-Khazragy

ABSTRACT

The survival rate of AML patients is remarkably low and this remains a challenge. Thus, finding novel treatments is urgently needed. Numerous studies have in-depth described how miRNA expression is frequently dysregulated in human acute myeloid leukemia (AML). This study aimed to evaluate the role of miR-155 gene silence on oncogenesis of acute myeloid leukemia cell lines via dysregulation of Src homology 2 domain containing inositol polyphosphate 5-phosphatase 1 (SHIP1) and CCAAT/enhancer binding protein beta (CEBPβ) genes expression to access the potential role of anti-miR-155 as a therapeutic target in acute myeloid leukemia. Total cell count and cell viability by using trypan blue staining assay showed a marked reduction of cell viability in miR-155 inhibitor transfected cells compared to MOCK cells. MTT assay showed that transfection of K562 cells with miR-155 inhibitor suppresses the cell proliferation and showed marked decline in tumor load. Moreover, cultured K562 cells showed marked reduction in the miR-155 gene expression level and marked increased in the CEBPB and SHIP1 genes expression levels compared to untreated cells. In conclusion the current study has validated the significance of knocked-down miR-155 expression in human AML cell line (K562). In addition, the current results suggested that miR-155 have an oncogenic role and inhibition of miR-155 was verified to have a tumor suppressive role. Thus miR-155 might be used as therapeutic target in acute myeloid leukemia patients in the future.