Background: Acute lymphoblastic leukemia (ALL) is known as a sort of malignancy in the blood lymphoid progenitors, specifically in B and T precursors of the lymphocyte. Autophagy is a protected hemostatic and catabolic process during evolution, through which lysosomes degrade the cytoplasmic components, such as redundant or dysfunctional organelles and misfolded proteins. We conducted the present study to investigate the link between gene expression changes of BECN1, MAP1LC3B, and P62 as the main regulators of remission and response to chemotherapy in ALL patients with minimal/measurable residual disease in ALL.
Method: In this case-control study, BECN1, MAP1LC3B, and P62 gene expression were assessed in 30 ALL patients at the diagnosis phase, 18 patients on day 15 of the therapy, and 11 controls employing qRT-PCR.
Results: The results revealed that BECN1and MAP1LC3B gene expression levels were significantly lower in ALL patients; whereas, P62 gene expression levels were significantly higher than the controls (P < 0.05). We found that the expression level of the BECN1 and P62 genes increased and decreased respectively in patients on day 15 of the therapy compared with newly diagnosed ALL patients. Nevertheless, neither BECN1 nor P62 genes were significantly different at the rate of 0.73-fold (P > 0.05).
Conclusion: Our study demonstrated the relationship between autophagy-related markers, such as BECN1, MAP1LC3B, and P62 with pathogenesis in Iranian children with ALL. We found that BECN1and MAP1LC3B genes significantly decreased in newly diagnosed ALL patients and may play a part in ALL pathogenesis.