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目的:探讨FZD5基因在前列腺癌骨转移中的作用机制,寻找前列腺癌骨转移的新的治疗方法。方法:检测前列腺癌PC3细胞内FZD5基因表达水平。将siRNA转染入PC3细胞后使FZD5基因沉默,继而观察PC3细胞迁移、增殖的变化。在此基础上通过小鼠胫骨注射建立前列腺癌骨转移模型,之后每周在胫骨腔内注射对照siRNA或FZD5基因沉默siRNA,于0、1和3周拍X平片观察肿瘤骨破坏,在3周后取材,行HE染色观察肿瘤骨破坏情况。结果:将FZD5基因沉默siRNA转染入前列腺癌PC3细胞后,细胞内FZD5基因表达量下降约70%。基因沉默组细胞增殖显著低于对照组(P<0.05)。FZD5基因沉默48 h后,细胞迁移能力较对照组下降了30%(P<0.05)。小鼠模型胫骨腔内注射对照siRNA或沉默siRNA 3周时,对照组和实验组均可见溶骨性破坏,但FZD5基因沉默组破坏相对较少,仍可见部分残留骨小梁。结论:通过抑制FZD5基因,可减少前列腺癌细胞的迁移和增殖,可能辅助减少前列腺癌患者的骨转移及骨破坏,从而提高患者的生存率及生活质量。其从分子生物学的角度为前列腺癌的发病机制以及治疗方法提供了新的思路。
Objective: To investigate the mechanism of FZD5 gene in the bone metastasis of prostate cancer and to search for a new therapeutic method for bone metastasis of prostate cancer. Methods: The expression of FZD5 gene in prostate cancer PC3 cells was detected. After transfection of siRNA into PC3 cells, the FZD5 gene was silenced, and then the changes of PC3 cell migration and proliferation were observed. On this basis, a model of prostate cancer bone metastasis was established by injecting mouse tibia, then control siRNA or FZD5 gene silencing siRNA was injected into the tibial cavity every week. X-ray films were taken at 0, 1 and 3 weeks to observe tumor bone destruction. Drawn weeks later, HE staining was performed to observe the tumor bone destruction. Results: The FZD5 gene silencing siRNA transfection into prostate cancer PC3 cells decreased the expression of FZD5 gene in cells by about 70%. The cell proliferation in gene silencing group was significantly lower than that in control group (P <0.05). FZD5 gene silencing 48 h, the cell migration ability than the control group decreased by 30% (P <0.05). Mouse model Tibia intracerebroventricular injection of control siRNA or silencing siRNA 3 weeks, the control group and the experimental group were seen osteolytic destruction, but the FZD5 gene silencing group is relatively less damage, still visible part of the residual trabecular. Conclusion: FZD5 gene can reduce the migration and proliferation of prostate cancer cells, which may help reduce the bone metastasis and bone destruction in patients with prostate cancer, thereby improving the survival rate and quality of life of patients. It provides a new idea for the pathogenesis and treatment of prostate cancer from the perspective of molecular biology.