Elucidating the genetic mechanism of anti-cancer efficacy of prednisolone in acute lymphoblastic leukemia through anti-miRNA treatments

Abstract

Background/aim

Acute lymphoblastic leukemia (ALL) is a form of hematological cancer that primarily affects children. Although agents such as prednisolone are used in the treatment of this disease, chemotherapy resistance remains a concern. This study aims to elucidate the genetic mechanism underlying the previously demonstrated anticancer efficacy of anti-miRNA therapies in ALL.

Materials and methods

Using IPA software, we identified genes targeted by miRNAs with demonstrated anticancer activity. For modeling ALL, SUP-B15 cells were employed, whereas NCI-BL2171 cells were used to represent healthy B lymphocytes. Commercial miRNA inhibitors and Lipofectamine were used to perform the transfection. RT-qPCR was used to assess target gene expression, and fold changes were calculated using the 2^-ΔΔCt method.

Results

In the SUP-B15 cell line, MYO10 gene expression was downregulated, whereas TAB2 gene expression was upregulated following the silencing of the ALL-related miRNAs in both ALL and healthy cell models. In the healthy NCI-BL2171 cell line, MYO10 gene expression was increased.

Conclusion

Genomic instability resulting from MYO10 dysregulation promotes tumor growth and contributes to immune checkpoint blockade. TAB2 plays a role in regulating the hematopoietic system, either directly or indirectly. Understanding the functions of these genes may provide valuable insights into the mechanisms underlying cancer and hematopoiesis, potentially leading to the development of new therapies for these conditions. The mechanisms of miRNA dysregulation in ALL remain to be elucidated, and anti-miRNA-based treatments need to be developed.