韩俊岭,陈 昆,马杰锋.沉默LMTK2对去势抵抗性前列腺癌PC3细胞增殖的影响[J].中国肿瘤,2019,28(1):63-68.
沉默LMTK2对去势抵抗性前列腺癌PC3细胞增殖的影响
Effect of LMTK2 on Proliferation of Castration-resistant Prostate Cancer PC3 Cells
投稿时间:2018-07-11  
DOI:10.11735/j.issn.1004-0242.2019.01.A009
中文关键词:  Lemur 酪氨酸激酶2  雄激素受体  去势抵抗性前列腺癌  PC3细胞
英文关键词:Lemur tyrosine kinase 2(LMTK2)  androgen receptor(AR)  castration-resistant prostate cancer(CRPC)  PC3 cells
基金项目:河南省2012年科技发展计划(122102310113);郑州市2015年度科技发展计划(20150064)
作者单位
韩俊岭 郑州人民医院 
陈 昆 郑州人民医院 
马杰锋 郑州人民医院 
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中文摘要:
      摘 要:[目的] 研究Lemur 酪氨酸激酶2(Lemur tyrosine kinase 2,LMTK2)在去势抵抗性前列腺癌(castration resistant prostate cancer ,CRPC)中对雄激素受体(androgen receptor,AR)的调节作用并提出可能的作用机制。[方法] 设计合成针对LMTK2基因的siRNA(siLMTK2),阴性对照siRNA(NC);采用瞬时转染法将以上siRNA转入前列腺癌PC3细胞,不转染的细胞设置为空白对照(Mock);采用Western blot检测转入LMTK2 siRNA对前列腺癌细胞及空白对照(Mock)中LMTK2蛋白表达的影响;通过克隆形成实验和细胞增殖实验考察沉默LMTK2基因对PC3细胞的肿瘤形成和增殖的影响。[结果] 研究发现沉默LMTK2基因后,前列腺癌PC3细胞中LMTK2 mRNA和蛋白质表达水平显著降低;相反地,雄激素相关基因的转录显著升高。另外,LMTK2基因沉默会导致PC3细胞成瘤能力和增殖能力增强,即致癌性增强。[结论] 本研究发现LMTK2是一种AR活性的负调节因子,沉默LMTK2基因能上调AR活性从而增强前列腺癌PC3细胞的增殖。这也为CRPC患者的治疗提供了一种新靶标,从而能够采取更有效的治疗方法。
英文摘要:
      Abstract:[Purpose] To investigate the effect of Lemur tyrosine kinase 2(LMTK2) gene on cell proliferation of castration-resistant prostate cancer (CRPC) and the possible mechanism. [Methods] LMTK2 siRNA was designed,synthesized and transfected into CRPC PC3 cells. The expression levels of LMTK2 protein in siLMTK2 and blank control group were detected by Western blot. The effects of LMTK2 on the tumor forming capacity and cell viability of PC3 cells were detected by tumor sphere assay and cell viability assay. [Results] After silencing LMTK2 gene in PC3 cells,the expression levels of LMTK2 protein and mRNA were significantly down-regulated,and the tumor forming capacity and proliferation were promoted. [Conclusion] Silencing LMTK2 gene may up-regulate AR activity leading to the proliferation of PC3 cells,which suggests that LMTK2 might be a novel therapeutic target for treatment of castration-resistant prostate cancer.
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