Mesalazine induces apoptosis via mitochondrial pathway in K562 cell line

Inflammation is an initial response of the body to infection and relationship between inflammation and cancer has been established. Nuclear factor kappa B (NF-κB) is a central factor in inflammation and its activity contributes to tumor progression and apoptosis prevention consequently leading to cancer promotion. As a result, NF-κB inhibitors can cause apoptosis. In this study, the effect of mesalazine as a NF-κB inhibitor on growth and apoptosis of K562 cells has been investigated. The K562 cells were first cultured in RPMI-1640 medium containing 10.00% fetal bovine serum. After that, they were treated for 72 hr with different concentrations of mesalazine (20.00, 40.00, 60.00 and 80.00 μM mL^-1). The MTT assay was used to evaluate cell viability. Hoechst staining and RT-PCR of apoptosis related genes (Bcl-2 and Bax) were carried out to illustrate apoptosis induction and immunocytochemistry was performed to investigate changes in c-Myc protein level. According to the results of MTT assay, all of applied mesalazine concentrations decreased K562 cells viability. Hoechst staining showed that the fragmented nuclei increased indicating apoptosis induction. Immuno-cytochemical ‎ results showed that mesalazine decreased c-Myc in treated cells. The RT-PCR results also showed an increase in Bax and a decrease in Bcl-2 expressions in mesalazine-treated cells. As the results suggest, mesalazine reduces cell viability by inducing apoptosis in K562 cell line; therefore, it can be used as a candidate for the leukemia treatment.