目的 探究 BX⁃912 对前列腺癌骨转移小鼠骨质破坏的影响。方法 体外实验：用递增浓度的BX⁃912干预小鼠前列腺癌细胞（RM⁃1），CCK⁃8检测BX⁃912对RM⁃1活性的影响，划痕实验观察BX⁃912对 RM⁃1 迁移的影响，克隆实验研究BX⁃912对RM⁃1独立生存能力的影响。体内实验：将30只前列腺癌骨转移 小鼠随机分为3组，分别为对照组、低浓度组、高浓度组，用相应浓度的BX⁃912干预，14 d后行Micro⁃CT检测并 称重瘤体，观察前列腺癌骨转移小鼠的骨质破坏情况。结果 CCK⁃8结果显示，BX⁃912浓度在0.625 μmol/L 及以下对RM⁃1活力无明显影响（P＞0.05），在1.25 μmol/L及以上对RM⁃1有明显抑制作用（P＜0.05）；划痕实验显示，BX⁃912能抑制RM⁃1的迁移能力（P＜0.05）；克隆实验表明，BX⁃912显著抑制RM⁃1的克隆形成率（P＜ 0.05）；体内实验表明，BX⁃912明显抑制前列腺癌的生长和骨质破坏（P＜0.05）。结论 BX⁃912能抑制RM⁃1 的增殖、迁移与克隆，并抑制前列腺癌骨转移小鼠的骨质破坏，有治疗前列腺癌骨转移前景。

Objective To investigate the effect of BX⁃912（PDK⁃1 Specific inhibitor）on bone destruction in mice with bone metastases in prostate cancer. Methods In vitro experiment：BX⁃912 was used to intervene in mouse prostate cancer cells（RM⁃1）with increasing concentrations，and the effect of BX⁃912 on the activity of RM⁃1 was detected by Cell Counting Kit⁃8（CCK⁃8），The effect of BX⁃912 on RM⁃1 migration was observed through cell scratch experiment，the effect of BX⁃912 on the independent viability of RM⁃1 was studied by cell cloning experi⁃ ment. In vivo experiment：30 mouse model of prostate cancer bone metastasis were randomly divided into three groups： the control group，the low concentration group，and the high concentration group. Each group was injected with the corresponding concentration of BX⁃912. After 14 days，the tumor was detected by micro⁃CT and weighed after resection. Results CCK⁃8 results showed that the BX⁃912 concentration at 0.625 μmol/L or below had no signifi⁃ cant effect on the activity of RM⁃1（P > 0.05），while the BX⁃912 concentration at 1.25 μmol/L or above had signif⁃ icant inhibitory effect on RM⁃1（P < 0.05）. The scratch test showed that BX⁃912 could significantly inhibit the mi⁃ gration of RM⁃1（P < 0.05）. The clone experiment showed that BX⁃912 significantly inhibited the clone formation rate of RM⁃1（P < 0.05）. BX⁃912 can significantly inhibit the growth of prostate cancer and inhibit the bone destruction in the mouse model of prostate cancer bone metastasis（P < 0.05）. Conclusion BX⁃912 can inhibit the proliferation，migration and cloning of RM⁃1 and ameliorate the bone destruction in the mouse model of bone metastasisin prostate cancer，which has potential significance for the treatment of bone metastasisin prostate cancer.