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BAY11-7082对前列腺癌细胞内NF-κB及其生物学行为的影响 被引量：1

Effects of BAY 11-7082 on NF-κB Expression and Its Biological Behaviors in Prostate Cancer Cells
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摘要 目的:探讨BAY11-7082对前列腺癌细胞NF-κB表达及其生物学行为的影响。方法:应用CCK-8方法、蛋白印迹、NF-κB激活-核转运检测,细胞增殖抑制实验和集落形成实验方法观察BAY11-7082作用下前列腺癌细胞NF-κB蛋白的表达,细胞生长等指标的变化。结果:BAY11-7082对前列腺癌细胞转移有明显的抑制作用。BAY11-7082处理的前列腺癌细胞内NF-κB蛋白表达降低,减弱NF-κB的激活,细胞增殖和形成集落的能力下降。结论:BAY11-7082可抑制前列腺癌细胞NF-κB的激活与表达,提示NF-κB可作为前列腺癌基因治疗的重要靶点之一。 Objective： This study was designed to determine the effect of BAY 11-7082 on NF-~cB expression and tumor colony formation of prostate cancer cells. Methods： Cell cytotoxicity assay kit-8 was used to detect cell death and proliferation according to the protocol. Western blot and densitometry analysis were performed to compare the expression of NF-KB in the control group with that of BAY 11-7082, an NF-nB inhibitor that is used to treat prostate cancer cells. Immunofluorescent staining was also conducted to moni- tor NF-KB activation and translocation in the nucleus. The effects of BAY 11-7082 on colony formation were determined by counting the number of prostate cancer cell colonies. Results： The treatment of prostate cancer cell line PC-3 cells by BAY 11-7082 inhibited cell proliferation and formed few colonies. Similarly, NF-tcB protein level dramatically decreased. Its translocation in the nucleus and the activation in the PC-3 cells were disrupted because of the effects of BAY 11-7082. Conclusion： BAY 11-7082 can inhibit the aberrant activation of NF-κB in prostate cancer cells and reduce tumor metastasis. Therefore, BAY 11-7082 is a potential drug for the treatment of prostate cancer patients in clinical practice in the future.
作者 钱敏 王世宣 王鸿雁 卢运萍 马丁 刘荣华
机构地区 华中科技大学同济医学院附属同济医院肿瘤生物医学中心教育部肿瘤侵袭与转移重点实验室 南京军区南京总医院妇产科
出处 《中国肿瘤临床》 CAS CSCD 北大核心 2012年第21期1608-1611,共4页 Chinese Journal of Clinical Oncology
基金 国家重点基础研究发展规划(973)项目(编号:2009CB521800)资助~~
关键词 前列腺癌 NF-ΚB BAY11-7082 转移 Prostatic neoplasm NF-κβ BAY 11-7082 Metastasis
分类号 R737.25 [医药卫生—肿瘤]
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参考文献16

  • 1Lamoureux F, Thomas C, Yin MJ, et al. A novel HSP90 inhibitor delays castrate-resistant PSA levels and inhibits prostate cancer without altering serum osteodastogenesis[J]. Clin Cancer Res,2011, 17(8):2301-2313.
  • 2Jain G, Cronauer MV, Schrader M, et al. NF-kB signaling in pros- tate cancer: a promising therapeutic target[J].? World J Urol, 2012, 30(3):303-310.
  • 3MinJ, Zaslavsky A, Fedele G, et al. An oncogene-tumor suppres- sor cascade drives metastatic prostate cancer by coordinately activat- ing Ras and nuclear factor-kappaB[J].Nat Med, 2010, 16(3): 286-294.
  • 4Kar S, Palit S, Ball WB, et al. Carnosic acid modulates Akt/IKK/ NF-kB signaling by PP2A and induces intrinsic and extrinsic path- way mediated apoptosis in human prostate carcinoma PC-3 cells [J]. Apoptosis, 2012, 17(7):735-747.
  • 5Vaccaro V, Melisi D, Bria E, et al. Emerging pathways and future targets for the molecular therapy of pancreatic cancer[J]. Expert Opin Ther Targets, 2011, 15 (10): 1183-1196.
  • 6Wu ST, Sun GH, Hsu GY, et al. Tumor necrosis factor-a induces epithelial-mesenchymal transition of renal cell carcinoma cells via a nuclear factor kappa B-independent mechanism[J].Exp Biol Med(Maywood), 2011, 236(9):1022-1029.
  • 7O'Neill AJ, Prencipe M, Dowling C, et al. Characterisation and ma- nipulation of docetaxel resistant prostate cancer cell lines[J].Mol Cancer, 2011, 10:126.
  • 8Zhu B, Liu Z, Wang P, et al. A nuclear factor-kappaB inhibitor BAY11-7082 inhibits interactions between human endothefial cells, T cells, and monocytes[J]. Transplant Proc, 2008, 40(8): 2724-2728.
  • 9Mendez-Samperio P, Trejo A, Perez A. Mycobacterium boris bacil- lus Calmette-Guerin induces CCL5 secretion via the Toll-like re- ceptor 2-NF-kappaB and-Jun N-terminal kinase signaling path- ways[J]. Cllin Vaccine Immunol, 2008, 15(2): 277-283.
  • 10Mahadevan NR, RodvoldJ, Almanza G, et al. ER stress drives Lipo- calin 2 upregulation in prostate cancer cells in an NF-kB-depen- dent manner[J].BMC Cancer, 2011, 11:229.

二级参考文献11

  • 1Kim KM, Lee K, Hong YS, et al. Fas-mediated apoptosis and expression of related genes in human malignant hematopoietic cell. Exp Mol Med, 2000; 32:246-254
  • 2Qin Y, Camoretti-Mercado B, Blokh L, et al. Fas resistance of leukemic eosinophils is due to activation of NF-kappa B by Fas ligation. J Immunol, 2002; 169: 3536-3544
  • 3Barnhart BC， Pietras EM， AlgecirasSchimnich A, et al. CD95 apoptosis resistance in certain cells can be overcome by noncanonical activation of caspase-8. Cell Death Differ, 2005;12:25-37
  • 4Meli M， D'Alessandro N， Tolomeo M, et al. NF-kappaB inhibition restores sensitivity to Fas-mediated apoptosis in lymphoma cell lines. Ann NY Acad Sci,2003;1010:232-236
  • 5Buzyn A,Petit F,Ostanko itch M,et al. Membrane-bound Fas(Apo-1/ CD95) ligand on leukemic cells:a mechanism of tumor immune escape in leukemic patients. Blood,1999;94:3135-3140
  • 6Barnhart BC, Legembre P, Pietras E, et al. CD95 ligand induces motility and invasiveness of apoptosis-resistant tumor cells. EMBO J, 2004; 23:3175-3185
  • 7Kavurma MM, Khachigian LM. Signaling and transcriptional control of Fas ligand gene expression. Cell Death Differ, 2003; 10:36-44
  • 8Savickiene J, Treigyte G, Magnusson KE, et al. p21(Waf1/Cip1) and FasL gene activation via Sp1 and NFkappaB is required for leukemia cell survival but not for cell death induced by diverse stimuli. Int J Biochem Cell Biol, 2005;37:784-796
  • 9Kater AP, Dicker F, Mangiola M, et al. Inhibitors of XIAP sensitize CD40-activated chronic lymphocytic leukemia cells to CD95-mediated apoptosis. Blood,2005; 106:1742-1748
  • 10Doyle BT, O'Neill AJ, Newsholme P, et al. The loss of IAP expression during HL-60 cell differentiation is caspaseindependent. J Leukoc Biol,2002; 71:247-254

同被引文献26

  • 1Wang HQ, Altomare DA, Skele KL, et al. Positive feedback regulation between Akt activation and fatty acid syathase expression in ovarian carcinoma cells[J]. Oncogene, 2005, 24(22): 3574-3582.
  • 2Zaidi N, Swinnen JV, Smans K. ATP-citrate lyase: a key player in cancer metabolism [ J ]. Cancer research, 2012, 72 ( 15 ): 3709 - 3714.
  • 3Xie J, Wu H, Dai C, et al. Beyond Warburg effect -- dual metabolic nature of cancer cells[ J/OL]. Sci Rep, 2014, 4 : 4927.
  • 4Zaidi N, Royaux I, Swinnen JV, et al. ATP citrate lyase knockdown induces growth arrest and apoptosis through different cell- and environment-dependent mechanisms [ J]. Mol Cancer Ther, 2012, 11(9) : 1925 -1935.
  • 5Migita T, Okabe S, Ikeda K, et al. Inhibition of ATP citrate lyase induces triglyceride accumulation with altered fatty acid composition in cancer cells[J]. Int J Cancer J, 2014, 135(1) : 37 -47.
  • 6Khwairakpam AD, Shyamananda MS, Sailo BL, et al. ATP citratelyase (ACLY): a promising target for cancer prevention and treatment[J]. Curt Drug Targets, 2015, 16(2) : 156 - 163.
  • 7Hanai J, Doro N, Sasaki AT, et al. Inhibition of lung cancer growth: ATP citrate lyase knockdown and statin treatment leads to dual blockade of mitogen-activated protein kinase ( MAPK ) and phosphatidylinositol-3-kinase ( PI3K )/AKTpathways [ J ]. J Cell Physiol, 2012, 227(4) : 1709 - 1720.
  • 8Migita T, Narita T, Nomura K, et al. ATP citrate lyase: activation and therapeutic implications in non-small cell lung cancer [ J ]. Cancer Res, 2008, 68 (20) : 8547 - 8554.
  • 9Zhou Y, Bollu LR, Tozzi F, et al. ATP citrate lyase mediates resistance of colorectal cancer cells to SN38 [ J ]. Mol Cancer Ther, 2013, 12(12) : 2782 -2791.
  • 10IJng J, Kumar R. between NF-KB and glucoctiedd signaling: a potential tmget breast case therapy[J]. Cancer Lett, 2012, 322(2) : 119 -126.

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中国肿瘤临床
2012年 第21期

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