Beclin1, Atg10 and Atg7 genes expressions as autophagy mediators in acute B-lymphoblastic leukemia

Abstract

Acute lymphoblastic leukemia (ALL), manifested by the rapid proliferation of blasts in the bone marrow, is the most prevalent pediatric malignancy; however, it could also be detected in the adults. Autophagy is a programmed catabolic process involved in the maintenance of cell homeostasis through destruction of damaged organs and misfolded proteins. Disruption of autophagy leads to abnormalities in cellular processes associated with cancer and acts as a double-edged sword. Although in a number of cancers, the suppression of autophagy resulted in a tumorigenesis process, in other types of this disease, the activation of this process may participate in the maintenance of cell survival. In this study, we evaluated the expression of Beclin1, Atg7 and Atg10 genes in 50 patients diagnosed with de novo B-ALL in comparison with 18 healthy counterparts using relative-quantitative real time-PCR. The majority of B-ALL patients showed a significant reduction in the expression of aforementioned genes as compared to the control group (P < 0.05). Moreover, we found a positive correlation between Beclin1 and Atg7 expression level in the patients (P < 0.001 and r = 0.57). These findings suggested that probably any disruption in the regulation of autophagy could be involved in leukemogenesis and thereby autophagy could be regarded as a valuable therapeutic target to eliminate the leukemic cells.