期刊文献+

肾母细胞瘤中Par-4的表达及过表达Par-4对肿瘤细胞的杀伤效应 被引量:3

Par-4 expression in Wilms Tumor and the killing effect of overexpressing Par-4 on tumor cells
下载PDF
导出
摘要 目的:研究肾母细胞瘤中Par-4的表达及过表达Par-4对肿瘤细胞的杀伤效应。方法:收集肾母细胞瘤组织及肿瘤旁正常组织,测定Par-4的表达量;培养SK-NEP-细胞,转染Par-4质粒后,测定Par-4的表达量、细胞生长情况以及凋亡相关基因的表达量。结果:肾母细胞瘤组织中Par-4的表达量显著低于肿瘤旁正常组织,不同组织分型肿瘤组织中Par-4的表达量无差异,TNM III-IV期、有淋巴结转移肿瘤组织中Par-4的表达量显著低于TNM I-II期、无淋巴结转移的肿瘤组织;转染不同浓度的Par-4质粒后,细胞的生长受到显著抑制,100μg/mL质粒的抑制效应最为显著;转染100μg/mL的Par-4质粒,NF-kB的表达量低于阴性对照组,FasL、Fas、Caspase-3、Caspase-8的表达量高于阴性对照组。结论:肾母细胞瘤中Par-4的表达量显著降低,过表达Par-4能够抑制肿瘤细胞的生长、具有杀伤效应。 Objective: To study the expression of Par-4 in Wilms Tumor and the killing effect of overexpressing Par-4 on tumor cells. Methods: Wilms Tumor tissue and adjacent normal tissue were collected to detect Par-4 expression levels. SK- NEP-1 cells were cultured and transfected with Par-4 plasmid, and then Par-4 expression levels, cell growth and expression levels of apoptosis-related genes were detected, Results: Par-4 expression levels in Wilms Tumor tissue were significantly lower than those in adjacent normal tissue. There was no significant difference in Par-4 expression levels in tumor tissue with different tissue typing, and Par-4 expression levels in tumor tissue with TNM III-IV stage and with lymph node metastasis were significantly lower than those in tumor tissue with TNM I-II stage and without lymph node metastasis. After transfection of different concentrations of Par-4 plasmid, cell growth was significantly inhibited, and the inhibitory effect of 100 μg/mL plasmid was the most significant~ after transfection of 100 μg/mL Par-4 plasmid, NF-kB expression levels were lower than those of negative control group, and expression levels of FasL, Fas, Caspase 3 and Caspase-8 were higher than those of negative control group. Conclusion.. Par-4 expression level significantly decreases in Wilms tumor, and overexpression of Par 4 can inhibit tumor cell growth and has killing effect.
出处 《海南医学院学报》 CAS 2016年第7期639-642,共4页 Journal of Hainan Medical University
基金 福州市科学技术局(2013Y6005)~~
关键词 肾母细胞瘤 前列腺凋亡应答蛋白4 凋亡 Wilms Tumor Prostate apoptosis response-4 Apoptosis
  • 相关文献

参考文献15

  • 1Zakaria OM, Hokkam EN, A1 Sayem K, et al. Primary Sur gery in Treatment of Stages Ⅱ and Ⅲ Wilms' Tumour.. A De- veloping Countries' Experience [J]. Gulf J Oncolog, 2015, 1 (19) :44-49. 被引量:1
  • 2Davidoff AM, Interiano RB, Wynn L, et al. Overall Survival and Renal Function of Patients With Synchronous Bilateral Wilms Tumor Undergoing Surgery at a Single Institution [J]. Ann Surg, 2015, 262(4): 570-576. 被引量:1
  • 3吴增丁,王冠林,张宽仁.前列腺凋亡应答蛋白4促凋亡和肿瘤特异性抑制作用的研究进展[J].南方医科大学学报,2014,34(1):128-132. 被引量:4
  • 4Yan-Fang T, Zhi-Heng L, Li-Xiao X, et al. Molecular Mecha- nism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells [J]. PLoS One, 2015, 10(7) : e0126566. 被引量:1
  • 5Qinan W, Ling Z, Bing C. PAR-4: a possible new target for age-related disease [J]. Expert Opin Ther Targets, 2014, 18 (8) :917-927. 被引量:1
  • 6Toska E, Roberts SG. Mechanisms of transcriptional regulation byWT1 (Wilms'tumour 1) [J]. BiochemJ, 2014, 461(1):15-32. 被引量:1
  • 7Liu Y, Liu S. Berberine inhibits Wilms" tumor cell progression through upregulation of Wilms' tumor gene on the X chromo some [J]. MolMedRep, 2013, 8(5): 1537 -1541. 被引量:1
  • 8Tao YF, Lu J, Du XJ, et al. Survivin selective inhibitor YM155 induce apoptosis in SK-NEP-1 Wilms tumor cells [J]. BMC Cancer, 2012, 26(12): 619. 被引量:1
  • 9Meynier S, Kramer M, Ribaux P, et al. Role of PAR-4 in o- varian cancer [J]. Oneotarget, 2015, 6(26):22641-22652. 被引量:1
  • 10Burikhanov R, Sviripa VM, Hebbar N, et al. Arylquins target vimentin to trigger Par-4 secretion for tumor cell apoptosis [J]. Nat Chem Biol, 2014, 10(11):924-926. 被引量:1

二级参考文献37

  • 1Global cancer facts& figures 2nd edition [M]. American cancer society, 2008: 4-9. 被引量:1
  • 2Cancer Facts& Figures[M]. American cancer society, 2012: 2-8. 被引量:1
  • 3Raft MC. Social controls on cell survival and cell death[J]. Nature, 1992, 356(6368): 397-400. 被引量:1
  • 4Steller H. Mechanisms and genes of cellular suicide [J]. Science, 1995, 267(5203): 1445-9. 被引量:1
  • 5Vanx DL, Haecker G, Strasser A. An evolutionary perspective on apoptosis[J]. Cell, 1994, 76(5): 777-9. 被引量:1
  • 6Hart LS, E1-Deiry WS. Cell death: a new Par-4 the TRAIL[J]. Cell, 2009, 138(2): 220-2. 被引量:1
  • 7Sells SF, Wood DP, Joshi-Barve SS, et al. Commonality of the gene programs induced by effectors of apoptosis in androgen-dependent and-independent prostate cells [J]. Cell Death Differ, 1994, 5(4): 457-66. 被引量:1
  • 8E1-Guendy N, Zhao Y, Gurumurthy S, et al. Identification of a unique core domain of par-4 sufficient for selective apoptosis induction in cancer cells[J]. Mol Cell Biol, 2003, 23(16): 5516-25. 被引量:1
  • 9Burikhanov R, Zhao Y, Goswami A, et al. The tumor suppressor Par-4 activates an extrinsic pathway for apoptosis [J]. Cell, 2009, 138(2): 377-88. 被引量:1
  • 10Hoffman RM. Clinical practice. Screening for prostate cancer[J]. N Engl J Med, 2011, 365(21): 2013-2019. 被引量:1

共引文献3

同被引文献18

引证文献3

二级引证文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部