Abstract

Objective Iron is an essential element for cell growing including tumor cells. This study aimed at investigating the effect of iron deprivation on HL-60 cell apoptosis. Methods HL-60 cells were cultured with different concentrations of ferric (Ⅲ) chloride (FeCL3), iron chelate-desferrioxamine (DFO), cytosine arabinoside (Ara-C), etoposide (VP-16), DFO+ Ara-C/VP-16, DFO+ FeCL3+ Ara-C/VP-16 for 6 hr, 12 hr, 24 hr and 48 hr. The proliferation of HL-60 cells was observed with cell viability assay. Apoptosis was determined with cell morphology, flow cytometry, DNA gel electrophoresis and the expression of c-myc. Results When HL-60 cells were incubated with different concentrations of FeCL3, apoptosis percentages (APO%) was lower than those in control group. The lowest percentage was found at the concentration of 100 μmol/L FeCL3. APO% of HL-60 in this group at 12 hr, 24 hr and 48 hr were 2.2±0.6, 3.7±1.6 and 6.1±1.3 respectively, while APO% in control group were 4.6±0.8, 5.2±1.4 and 10.3±1.9 (P 0.05). Expression percentage of c-myc in DFO group was higher than that of control group. At the concentration of 100 μmol/L DFO, expression percentage at 6 hr, 12 hr and 24 hr were 4.1±1.2, 18.3±4.1 and 53.4±7.0 respectively (P<0.05). Conclusion These results showed that iron could promote HL-60 cells growth and inhibit their apoptosis. Otherwise iron deprivation could induce HL-60 cell apoptosis. DFO disturbed the iron metabolism and inhibited DNA synthesis of HL-60 cells. This action of DFO might enhance the suseeptbility of HL-60 cells to apoptosis induced by chemotherapeutic drugs. Equal molar concentration of FeCL3 could prevent the effect of DFO. Our report showed that the iron deprivation could have a place in the treatment of leukemia in combination with other anticancer agents. Therefore we suggest that as long as the hemoglobin level is maintained sufficiently for survival of leukemia patients, red cell transfusion may not be necessary. Key words: Desferrioxamine; Apoptosis; Genes, myc

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