目的　探讨Bax基因的过表达是否能够调节HCC 92 0 4细胞系对阿霉素的敏感性。方法　采用一种可诱导性表达系统、MT Ⅱ调节系统 ,在外加锌离子 (ZnSO4,10 0 μmol/L)的条件下 ,诱导Bax基因过表达。以克隆形成实验来判断Bax是否能够降低阿霉素处理后肿瘤细胞的克隆存活率。以MTT实验来反映细胞活力的改变。凋亡性细胞死亡的鉴定是通过形态学标准并结合TUNEL和细胞周期的分析加以证实。结果　阿霉素能够显著诱导HCC 92 0 4细胞发生凋亡。TUNEL染色显示典型的凋亡特征如新月体样或环状染色体边集于核膜 ,胞浆皱缩并且“发泡”。流式细胞仪分析显示 ,在处理后 2 4h出现显著的亚二倍体峰。Bax能够显著降低阿霉素处理组的克隆存活率 ,Bax也能够降低药物处理后的细胞活力 ,呈时间依赖性。结论　Bax基因的过表达能够增加HCC 92 0 4对阿霉素杀伤作用的敏感性 Objective To investigate whether Bax gene overexpression can modulate the sensitivity of doxorubicin to HCC 92 0 4 cell line. Methods An inducible expression system and MT Ⅱ regulatory system were used to induce the overexpression of Bax gene under the condition of zinc sulfate (ZnSO4, 10 μmol / L). Clone formation assay was used to determine whether Bax could reduce the clonality of tumor cells after doxorubicin treatment. To MTT experiments to reflect changes in cell viability. The identification of apoptotic cell death was confirmed by morphological criteria combined with TUNEL and cell cycle analysis. Results Adriamycin significantly induced apoptosis in HCC 92 0 4 cells. TUNEL staining revealed typical apoptotic features such as crescent-like or ring-shaped chromosomes clustering on the nuclear membrane, cytoplasm shrinking and “foaming.” Flow cytometry analysis showed significant sub-diploid peaks at 24 h after treatment. Bax can significantly reduce the clonality of doxorubicin-treated group, and Bax can also reduce the cell viability after drug-treatment in a time-dependent manner. Conclusion Overexpression of Bax gene can increase the sensitivity of HCC 92 0 to doxorubicin killing