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FGF21对HepG2细胞TGF-β信号通路的影响 被引量:1

Effect of FGF21 in TGF-β Signaling Pathway of HepG2 Cells
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摘要 目的研究FGF21对TGF-β/Smads信号通路中相关蛋白和mRNA表达的影响。方法采用Western blot法检测HepG2 cells的TGF-1,TGF-βRⅡ,Smad 2,3,4,7的蛋白表达水平和采用Q-PCR方法检测HepG2 cells的TGF-β1,TGF-βRⅡ,Smad 2,3,4,7的mRNA表达水平。结果在不同FGF21浓度下,TGF-β1,TGF-βRⅡ,Smad 2,3,4,7蛋白和mRNA表达水平不同(P<0.05)。结论 FGF21通过促进TGF-β信号通路中的信号分子或受体的表达,或者通过下调此信号通路的阻断分子而抑制肿瘤发生。 OBJECTIVE To study the effects of FGF21 on relative proteins and mRNA expression involved inTGF-β/Smads signaling pathway. METHODS Detect the protein expressions of TGF-β1, TGF-β R Ⅱ, Smad 2,3,4,7 of HepG2 cells with Western blot and detect the mRNA expression of TGF-β1, TGF-β RⅡ, Smad 2, 3, 4, 7 of HepG2 cells with Q-PCR. RESULTS The expressions of the protein and mRNA of TGF-β1, TGF-β RⅡ, Smad 2, 3, 4, 7 varied with the different concentrations of FGF21(P〈0.05). CONCLUSION FGF21 might inhibit tumor by promoting TGF-β signaling pathway in the expression of signaling molecules or receptors, or by decreasing the blocking molecules of this signaling pathway.
出处 《中国现代应用药学》 CAS CSCD 2012年第8期675-678,共4页 Chinese Journal of Modern Applied Pharmacy
基金 浙江省教育厅科研项目(Y200907097)
关键词 FGF21 HEPG2细胞 SMAD FGF21 HepG2 cells Smad
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  • 1ITOH N, ORNITZ D M. Evolution of the fgfr gene families [J]. Trends Genet, 2004, 20(11): 563-569.
  • 2BEACHY P A, KARHADKAR S S, BERMAN D M. Mending and malignancy [J]. Nature, 2004, 431(7007): 402-406.
  • 3FENG X H, DERYNCK R. Specificity and versatility in TGF-beta signaling through Smads [J]. Annu Rev Cell Dev Biol, 2005, 21(15): 659-693.
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  • 6DUPONT S, MAMIDI A, CORDENONSI M, et al. FAM/ USP9x, a deubiquitinating enzyme essential for TGF-beta signaling, controls Smad 4 monoubiquitination [J]. Cell, 2009, 136(1): 123-135.
  • 7HOOVER L L, KUBALAK S W. Holding their own: the noncanonical roles of Smad proteins [J]. Sci Signal, 2008, 1(46): 135-144.
  • 8KAWATE S, TAKENOSHITA S, OHWADA S, et al. Mutation analysis of transforming growth factor beta type II receptor, Smad 2, and Smad 4 in hepatocellular carcinoma [J]. IntJ Oncol, 1999, 14(1): 127-131.
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同被引文献8

  • 1ITOH N, ORNITZ D M. Evolution of the fgfr gene families [J] Trends Genet, 2004, 20(11): 563-569.
  • 2BEACHY P A, KARHADKAR S S, BERMAN D M. Mending and malignancy [J]. Nature, 2004, 431(7007): 402.
  • 3FENG X H, DERYNCK R. Specificity and versatility in tgf-beta signaling through Smads [J]. Annu Rev Cell Dev Biol, 2005(21): 659-693.
  • 4PARSONS R, MYEROFF L L, LIU B, et al. Microsatellite instability and mutations of the transforming growth factor beta type III receptor gene in colorecta! cancer [J].Cancer Res, 1995, 55(23): 5548-5550.
  • 5MARKOWITZ S, WANG J, MYEROFF L, et al. Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability [J]. Science, 1995, 268(5215): 1336- 1338.
  • 6DUPONT S, MAMIDI A, CORDENONSI M, et al. FAM/ USP9x, a deubiquitinating enzyme essential for TGF-beta signaling, controls Smad4 monoubiquitination [J]. Cell, 2009, 136(1): 123-135.
  • 7HOOVER L L, KUBALAK S W. Holding their own: the noncanonical roles of Smad proteins [J]. Sci Signal, 2008, 1(46) : pe48.
  • 8KAWATE S, TAKENOSHITA S, OHWADA S, et al. Mutation analysis of transforming growth factor beta type II receptor, Smad2, and Smad4 in hepatocellular carcinoma [J]. Int J Oncol, 1999, 14(1): 127-131.

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