【Objective】 To explore the pivotal role of ABT737

a BH3 mimetic small molecule inhibitor

in enhancing radiosensitivity and its mechanism. 【Methods】 MTT assay was conducted to determine the inhibition rate of ABT737 in HeLa cells. The radiosensitizing effect of ABT737 in HeLa cells was detected by cell colony assay. The DNA damage of HeLa cells was examined by detection of histone variant H2AX (γ-H2AX) foci using indirect immunofluorescence. Flow cytometry with Annexin V-PI staining was used to assess the apoptosis. The expression of apoptotic proteins caspase-3 and PARP were detected using Western blot analysis. 【Results】 ABT737 significantly inhibited cell growth of HeLa cells with IC50 value of 15.7 μmol/L. Result of the colony formation assay indicated that the clonogenic survival of HeLa cells was decreased after combining the radiation. The DEF values for both combination groups were over one: 1.88 for the group treated with 8 μmol/L ABT737and 1.13 for the group treated with 12 μmol/L ABT-737. The survival fraction (SF) values for the group treated with 8 μmol/L ABT737 and the group treated with 12 μmol/L were 0.84 and 0.82

respectively. ABT737 increased the number of γ-H2AX focis and the cells that detected γ-H2AX foci in HeLa cells exposed radiation. After 24 h

γ-H2AX focis disappeared in radiation group

but the accumulation of γ-H2AX focis was also observed after combining ABT737. The expression levels of both cleaved-Caspase-3 and cleaved-PARP and the apoptotic rate of HeLa cells were increased in the combination group comparing to those in the groups that were treated with only ABT-737 or radiation. 【Conclusion】 Our data imply that ABT-737 can enhance radiosensitizing effects in human cervical cancer HeLa cells via delaying DNA damage repair after radiation and inducing apoptosis.