Background: Chronic myeloid leukemia (CML) is characterized by a reciprocal translocation t(9;22)
and forms BCR/ABL1 fusion gene called the Philadelphia chromosome. The therapeutic targets for CML patients
mediated with BCR/ABL1 oncogenic are tyrosine kinase inhibitors such as imatinib, dasatinib, and nilotinib. The
latter two of which have been approved for the treatment of imatinib-resistant or intolerance CML patients.
Mitotic catastrophe (MC) is one of the non-apoptotic mechanisms initiated in types of cancer cells in response to
anti-cancer therapies. Pharmacological inhibitors of G2 checkpoint members or genetic suppression of PLK1,
PLK2, ATR, ATM, CHK1, and CHK2 can trigger DNA-damage-stimulated mitotic catastrophe. PLK1 and
AURKA/B are anomalously expressed in CML cells, where phosphorylation and activation of PLK1 occur by
AURKB at centromeres and kinetochores.
Objective: The purpose of this study is to investigate the effect of dasatinib on the expression of genes in MC and
apoptosis pathways in K562 cells.
Methods: Total RNA was isolated from K-562 cells treated with the IC50 value of dasatinib and untreated cells as
a control group. The expression of MC and apoptosis-related genes, was analyzed by the qRT-PCR system.
Results: The array-data demonstrated that dasatinib-treated K562 cells significantly caused the decrease of
several genes (AURKA, AURKB, PLK, CHEK1, MYC, XPC, BCL2, and XRCC2).
Conclusion: The evidence supplies a basis to support clinical researches for the suppression of oncogenes such
as PLKs with AURKs in the treatment of types of cancer, especially chronic myeloid leukemia.