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目的：探讨甲基硒酸（methylseleninic acid，MSA）对前列腺癌Lncap细胞促凋亡效应，并初步探讨发生机制。方法将体外培养的Lncap细胞分为4组，即空白对照组（mock），MSA低剂量组（1.25μM）、中剂量组（2.50μM）和高剂量组（5.00μM），MSA分别作用24h、48h和72h，倒置显微镜下观察细胞形态，SRB法检测细胞增殖情况；流式细胞术检测细胞周期及凋亡；免疫荧光及免疫细胞化学法检测细胞内stat3的表达。结果光镜及SRB实验结果显示：随MSA剂量增加及作用时间延长，Lncap细胞生长受到明显抑制；流式细胞术结果表明：MSA呈剂量及时间依赖关系促进细胞凋亡，并使细胞周期分布发生改变，多数细胞被阻滞于G0~G1期；免疫荧光及免疫组织化学结果发现：与对照组相比，MSA可明显抑制细胞内stat3表达。结论 MSA抑制细胞增殖并促进细胞凋亡，其发生机制可能与降低stat3表达，进而抑制下游增殖基因表达有关。“,”Objective To investigate the proapoptotic effects of methylseleninic acid (MSA) on prostatic cancer Lncap cells and explore its mechanism. Methods The treated Lncap cells were divided into four groups such as the control group (mock), MSA low-dose group (1.25μM), middle dose group (2.50μM) and high dose group (5.00μM) respectively. Cell morphology was observed with microscope at the time of 24h, 48h and 72h after treatment. Cell proliferation was detected by SRB assay. Cell cycle and apoptosis was measured by flow cytometry. Stat3 expression was detected by immunofluorescence and immunocytochemical analysis. Results Light microscopy observation and SRB results indicated that the growth of Lncap cells were inhibited obviously with MSA dose and time dependent effect. Flow cytometry analysis showed that MSA promoted LNCap cells apoptosis with dose and time dependent effect and changed the cell cycle distribution. The majority of cells were arrested in G0-G1 phase. Immunofluorescence and immunohistochemistry results showed MSA could inhibit the expression of intracellular stat3 compared with that of the control group. Conclusion MSA might inhibit cell proliferation and induce apoptosis, and its mechanism was associated with decreased stat3 expression.