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肿瘤坏死因子-α诱导对膀胱癌细胞株NF-κB信号通路分子表达及细胞增殖水平的影响 被引量:2

Effects of tumor necrosis factor-αinduction on molecular expression of NF-κB signaling pathway and cell proliferation level in bladder cancer cell lines
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摘要 目的探讨肿瘤坏死因子-α(TNF-α)诱导对膀胱癌细胞株细胞核因子-κB(NF-κB)通路分子表达及细胞增殖水平的影响,为临床提供参考,以提高膀胱癌的治疗水平。方法选取膀胱癌细胞株T24、5637作为研究对象,根据处理的情况分为对照组和TNF-α处理组,其中对照组未采用TNF-α处理,TNF-α组经TNF-α处理,比较TNF-α处理对不同膀胱癌细胞株RelA、RelB基因的表达情况及膀胱癌细胞增殖活性的影响。结果 TNF-α处理T24细胞株后,TNF-α处理组的RelA、RelB基因表达均高于对照组(P<0.05);TNF-α处理5637细胞株后,RelA基因表达水平在作用3 h后明显上升(P<0.05),但是RelB基因表达水平与对照组相比差异无统计学意义(P>0.05)。对照组、TNF-α处理组T24和5367细胞株的存活率相比,差异均无统计学意义(P>0.05)。结论 TNF-α可诱导膀胱癌细胞NF-κB信号通路RelA、RelB基因的表达,对于细胞增殖的活性尽管有一定的影响,但是不明显。 Objective To investigate the effect of tumor necrosis factor-α(TNF-α)induction on the molecular expression of nuclear factor-κB(NF-κB)pathway and cell proliferation level in bladder cancer cell lines so as to provide reference for clinic and improve the treatment level of bladder cancer.Methods Bladder cancer cell lines T24 and 5637 were selected as the research objects and divided into the control group and TNF-αtreatment group according to the treatment conditions.The control group was not treated with TNF-α,and the TNF-αgroup was treated with TNF-α.The effects of TNF-αtreatment on the expression levels of RelA and RelB in different bladder cancer cell lines and the cell proliferation activities were compared between the two groups.Results After TNF-αtreatment in T24 cell lines,the levels of RelA and RelB gene expression in the TNF-αtreatment group were higher than those in the control group(P<0.05).After TNF-αtreatment in 5637 cell lines,the RelA gene level after 3 h of treatment was significantly increased(P<0.05),but the RelB gene level had no statistically significant difference compared with that in the control group(P>0.05).There was no statistically significant difference in the survival rate of T24 and 5367 cell lines between the control group and TNF-αtreatment group(P>0.05).Conclusion TNF-αcan induce the expression of the RelA and RelB genes in the NF-κB signaling pathway of bladder cancer cells,although which has a certain influence on the cellular proliferation activity,but which is unobvious.
作者 路蔓 付强 张静 LU Man;FU Qiang;ZHANG Jing(Department of Clinical Laboratory,Second Affiliated Hospital of Air Force Military Medical University,Xi′an,Shaanxi 710038,China;Department of Urological Surgery,Second Affiliated Hospital of Air Force Military Medical University,Xi′an,Shaanxi 710038,China)
出处 《检验医学与临床》 CAS 2021年第15期2145-2147,2151,共4页 Laboratory Medicine and Clinic
基金 陕西省重点研发计划一般项目-社会发展领域(S2020-YF-YBSF-0590)。
关键词 膀胱癌 肿瘤坏死因子-Α 核因子-ΚB 细胞增殖 bladder cancer tumor necrosis factor-α nuclear factor-κB cell proliferation
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  • 1叶小卫,叶会丽,陈瑶,陈林香,陈雪馨.亚砷酸对人肺腺癌细胞株TNF-α、Fas、bcl-2表达的影响[J].中药新药与临床药理,2007,18(4):273-275. 被引量:1
  • 2Aggarwal B, Vijayalekshmi R, Sung B. Targeting inflammatory pathways for prevention and therapy of cancer: short - term friend, long - term foe [ J ]. Clin Cancer Res, 2009, 15 (2) : 425 - 430.
  • 3Michaud D. Chronic inflammation and bladder cancer [ J ]. Urol Oncol, 2007, 25 (3) : 260 - 268.
  • 4Qiao L, Zhang H, Yu J, et al. Constitutive activation of NF -kap- paB in human hepatocellular carcinoma: evidence of a cytoprotec- tire role[J]. Hum Gene Ther, 2006, 17(3) : 280 -290.
  • 5Sub J, Rabson A. NF -kappaB activation in human prostate canc- er: important mediator or epiphenomenon? [ J]. J Cell Biochem, 2004, 91(1): 100-117.
  • 6Shen M, Duan X, Zhou P, et al. Lymphotoxin 13 receptor activa- ting nuclear factor - KB pathwaypromotes bladder cancer [ J ]. Molecu Med Rep, 2015, 11 (2): 783 -790.
  • 7Karin M. NF- kappaB as a critical link between inflammation and cancer [ J]. Cold Spring Harb Perspect Biol, 2009, 1 (5) : a000141.
  • 8Sethi G, Sung B, Aggarwal B. TNF : a master switch for inflamma- tion to cancer [ J]. Front Biosci, 2008, 13 ( 13 ) : 5094 - 5 107.
  • 9周永芹,韩莉.NF-κB与肿瘤关系的研究进展[J].现代肿瘤医学,2008,16(5):855-858. 被引量:8
  • 10夏启松,刘静维,孙仁宇,修瑞娟.大黄素对人肺腺癌A549细胞体外增殖凋亡及VEGF和TNF-α分泌的影响[J].肿瘤防治研究,2010,37(4):387-391. 被引量:10

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