～(131)I-GMCSF Induce Apoptosis Of HL-60

Objective The current study was designed to investigate the effect and mechanism of apoptosis of HL-60 cells induced by 131I-GMCSF, and to estimate the value of targeted radiopharmaceutic therapy in patients with acute myeloblastic leukemia (AML). Method we employed an in vitro radioimmunotherapy(RAIT)model. Data were collected from tetrazolium microculture (MTT) cellular cytotoxicity test, TUNEL technology, transmission electron microscopy, flow cytometric analysis and immunocytochemistry assay. Results when the radiative dose was higher than 18.5×108Bq/L, cell survival rate was markedly decreased, while cell apoptosis rate was significantly increased and cellar ultrastructure was markedly destroyed by 131I-GMCSF. G2/M cell-cycle arrest and loss of mitochondrial transmembrane potential (MTP) was founded in cells treated with 131I-GMCSF . The p53 was up regulated,while bcl-2 and bcl-xl was decreased. Conclusion These results show that 131I-GMCSF can induce HL-60 significant apoptosis through opening the mitochondrial permeability transition pore and reducing MTP, which suggests that 131I-GMCSF may be available in therapy of AML.