A preliminary study on the econazole induced endoplasmic reticulum related apoptosis in HL-60 leukemic cells

Objective: To investigate the anti-leukemic function of econazole (Ec), an azole anti-fungal drug. Methods: We compared efficacy of econazole to induce apoptosis in HL-60 cells with two other known endoplasmic reticulum (ER) stress inducer thapsigargin (Tg) and tunicamycin (Tu). Results: Cells treated with Ec showed typical morphology of apoptosis following 24 h incubation, parallel to the morphological changes, the expression of molecular chaperone GRP 78 was up-regulated in all cases and the caspase 12, an ER resident caspase was activated. Conclusion: Ec induced ER stress related apoptosis in HL- 60 cells; the underlying mechanisms are protein synthesis inhibition through eIF2α phosphorylation and caspase 12 activation.

Objective： To investigate the anti-leukemic function of econazole （Ec）, an azole anti-fungal drug. Methods： We compared efficacy of econazole to induce apoptosis in HL-60 cells with two other known endoplasmic reticulum （ER） stress inducer thapsigargin （Tg） and tunicamycin （Tu）. Results： Cells treated with Ec showed typical morphology of apoptosis following 24 h incubation, parallel to the morphological changes, the expression of molecular chaperone GRP 78 was up-regulated in all cases and the caspase 12, an ER resident caspase was activated. Conclusion： Ec induced ER stress related apoptosis in HL-60 cells; the underlying mechanisms are protein synthesis inhibition through eIF20α phosphorylation and caspase 12 activation.