MicroRNA-520a attenuates proliferation of Raji cells through inhibition of AKT1/NF-κB and PERK/eIF2α signaling pathway.

Burkitt's lymphoma (BL) is a fast growing cancer of the human lymphatic system, and an extremely invasive B-cell non-Hodgkin's lymphoma. We explored the mechanism of apoptosis in Raji cells associated with the post-transcriptional regulation factors. To confirm that the predicted microRNA-520a (miR-520a) is matched with AKT1, 3 untranslated region (UTR) luciferase activity of AKT1 was used in the assessment. In the presence of the mimics or inhibitors of miR-520a, cell function of Raji, such as proliferation, growth and apoptosis were analyzed. The expression of endoplasmic reticulum (ER) stress-related proteins were examined. Luciferase reporter analysis showed that miR-520a leads to decreased activity of luciferase gene fused with AKT1 3UTR. Therefore, AKT1 is a direct target of miR-520a. Our data indicated that the mimics of miR-520a inhibited growth, proliferation of Raji cells and promoted its apoptosis, which was related to downregulation of AKT1, NF-B and ER stress response mediated by PERK/eIF2 pathway. On the contrary, the inhibitors of miR-520a promoted growth, proliferation of Raji cells and inhibited its apoptosis, which was related to AKT1/NF-B and PERK/eIF2 pathway. We identified miR-520a, which specifically binds to AKT1 mRNA 3UTR. miR-520a is a crucial mediator for proliferation and ER stress in Raji cells through regulating the AKT1/NF-B or PERK/eIF2 signaling pathway. Our findings suggest that targeting miR-520a is a promising therapeutic strategy in BL.