[en] Objective: 17-allylamino-17-demethoxygeldanamycin(17-AAG) is a less toxic analogue of geldanamycin (GA) that retains the tumoricidal features of GA. Same as its parent compound, 17-AAG inhibits several signaling pathways through binding to heat shock protein (HSP) 90, which results in destabilization of signaling complexes and degradation of client proteins in a variety of tumor cell growth. Treatment with 17-AAG was effective to inhibit tumor growth and induce apoptosis in colon cancer, glioblastoma, and breast cancer cell lines. This study aimed at exploring the anti-proliferation effects and mechanism of ¹³¹I labeled 17-AAG on human breast cancer cell line MCF-7. Methods: ¹³¹I-17-AAG was prepared by the reaction of 17-AAG with Na¹³¹I in the presence of hydrogen peroxide. The MCF-7 cells were divided into 5 groups with different additional drugs: group A, dimethyl sulfoxide (DMSO); group B, 370 kBq Na¹³¹I; group C, 2.5 mg/L 17-AAG; group D, 370 kBq ¹³¹I-17-AAG; group E, 370 kBq ¹³¹I-17-AAG + 2.5 mg/L 17-AAG. 3- (4,5-dimethylthiazol-2-yl)-2,5, diphenylte-trazolium bromide (MTT) assay was used to evaluate the effect of growth inhibition of MCF-7 cells. Cell cycle and apoptosis were analyzed by flow cytometry. The change of the expression of Akt2 mRNA in MCF-7 cells was examined by RT-PCR. Results: The labeling yield of ¹³¹I-17-AAG was 83%. The radiochemical purity of ¹³¹I-17-AAG after purification was 96.6%. The specific activity was 1.48 x 10⁵ MBq/μmol. All drugs could significantly inhibit the growth of MCF-7 cells in vitro as the duration lasts longer, especially for group E. After 48 h, sub-G1 peaks detected by flow cytometry were(1.54±0.13)%, (5.72±1.05)%, (12.97±1.44)%, (20.65±1.36)%, (35.39±4.15)% for group A, B, C, D and E, respectively. The experimental groups (B-E) were all significantly higher than the control group (A, all P<0.05). The expression of Akt2 mRNA in treated MCF-7 cells (groups C-E) were all lower than that of the control group (A), especially for group E. Conclusions: ¹³¹I-17-AAG could suppress the growth of human breast cancer cell line MCF-7 and hasten the apoptosis. It could significantly suppress the expression of Akt2 mRNA. Combined with 17-AAG, ¹³¹I-17-AAG could improve the effect of radiotherapy. (authors)