Newly modified ciprofloxacin causes G0/G1 cell cycle arrest and apoptosis in human leukemia K562 cells via down-regulation of Bcl2 and survivin

Ciprofloxacin (CP) is an antibiotic with low side effects, which have anti-proliferative and apoptotic activities in numerous cancer cell lines. Prior studies indicated several CP derivatives, displayed higher in vitro anticancer activity than parent CP anticancer activity. Here, the anti-proliferative and apoptosis- inducing effects of a new modified CP, 1-isopropyl 4-methyl ciprofloxacin (IMC), was examined in human chronic myeloid leukemia (CML) K562 cell line.METHODS:Chronic myeloid leukemia K562 cells were treated with different concentration (10-120 ʽM) of IMC and cell viability determined by MTT assay. Induction of apoptosis evaluated morphologically by fluorescence microscope, as well as cell cycle analysis. Expression levels of some anti-apoptotic genes including Bcl-2 and Survivin were analyzed by qRT-PCR.RESULTS:IMC mediated growth inhibition in a dose- and time-dependent in the K562 cells. G0/G1 cell cycle arrest was showed after treatment of the cells with IC50 value (20 ʽM) of the compound. Furthermore, the qRT-PCR analysis revealed that treatment of the K562 cells with IMC down-regulates the expression of Bcl-2 and Survivin.CONCLUSION:According to the present data, it looks that this new modified CP is a good candidate for further evaluation as an effective chemotherapeutic drug in CML.

کلیدواژه ها:

Ciprofloxacin ، Apoptosis ، Chronic myeloid leukemia ، Bcl-2 ، Survivin.