Objective      To determine the effect of down-regulation of forkhead box protein M1 (FoxM1) on the cisplatin sensitivity of human laryngeal carcinoma Hep-2 cells and investigate the potential mech

anisms.       Methods      Small interfering RNA (siRNA) and FoxM1 inhibitor thiostrepton were used respectively to suppress FoxM1 expression in Hep-2 cells. The expression of FoxM1 at mRNA and protein levels was detected by qRT-PCR and Western blotting respectively. Cell viability and apoptosis of Hep-2 cells were detected by MTT assay and flow cytometry. Furthermore

qRT-PCR and Western blotting were used to investigate the changes of FoxM1 in Hep-2 cells with FoxM1 suppression and cisplatin treatment. The changes of apoptosis-related proteins were detected by Western blotting.       Results      Both of siRNA and thiostrepton suppressed FoxM1 expression

reduced the cell survival after cisplatin treatment and IC

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(cisplatin treated normal cells IC

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=2.609±0.102  g/mL

siRNA infected cells IC

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=0.771±0.058  g/mL

P0.05; cisplatin treated cells IC

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=2.142±0.198  g/mL

thiostrepton treated cells IC

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=0.773±0.063  g/mL

P0.05). The apoptotic rate was (4.197±0.273)%

(12.553±0.183)%

(37.465±4.305)% and (82.373±7.214) % respectively in the normal Hep-2 cells and the cells with siRNA infection

cisplatin treatment and infection plus cisplatin treatment

with that of the latter group of cells the highest (P0.05). The rate was (2.343 3±0.193 6)%

(10.127±0.479)%

(35.075±1.995)% and (62.843±1.824)% separately in the normal Hep-2 cells and the cells after thiostrepton treatment

cisplatin treatment and thiostrepton plus cisplatin treatment

with that of the latter group of cells the highest (P0.05). Down-regulation of FoxM1 inhibited the expression of Bcl-2 and up-regulated that of Bax.       Conclusion      FoxM1 promotes the sensitivity of Hep-2 cells to cisplatin

which potentially is due to its down-regulation of Bcl-2 and up-regulation of Bax.