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Leptin促进人脑胶质瘤生长及其机制研究 被引量:2

The increase in the growth of human glioma induced by leptin and its corresponding mechanism
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摘要 目的:研究瘦素(leptin)对人脑胶质瘤生长的影响,并探讨其分子机制。方法:以不同浓度leptin刺激人脑胶质瘤细胞U87-MG后,MTT法检测其细胞增殖的变化,FCM法检测leptin对U87-MG细胞周期及凋亡的影响;Real-time PCR法及Western印迹法检测leptin作用后,U87-MG细胞中信号转导和转录激活因子3(signal transducers and activators of transcription 3,STAT3)的表达;建立裸鼠皮下成瘤模型,进一步检测leptin对人脑胶质瘤裸鼠移植瘤生长及STAT3表达的影响。结果:Lep-tin可以显著促进人脑胶质瘤细胞U87-MG的体外生长,并呈剂量依赖性和时间依赖性;leptin促进U87-MG细胞由G0/G1期向S期转变,但对细胞凋亡无任何影响;U87-MG细胞中STAT3 mRNA和蛋白表达水平被显著提高。裸鼠皮下成瘤实验提示,leptin可以显著促进U87-MG细胞移植瘤生长,并提高移植瘤组织中STAT3的表达水平。结论:Leptin可以显著促进人脑胶质瘤生长,其作用机制可能与JAK2-STAT3信号转导通路的活化有关。 Objective:To investigate the effect of leptin on the growth of human glioma,and to elucidate its molecular mechanism.Methods:U87-MG human glioma cells were treated with different concentrations of leptin,and the cell proliferation was detected by MTT assay.The effects of leptin on cell cycle and apoptosis of U87-MG were analyzed by flow cytometry.Real-time PCR and Western blot were used to detect the expressions of signal transducers and activators of transcription 3(STAT3) in U87-MG cells.The subcutaneous tumor model in nude mice was used to further detect the effects of leptin on the growth of human glioma xenografts and expression of STAT3 in vivo.Results:Leptin significantly increased the growth of U87-MG human glioma cells in a dose-dependent and time-dependent manner.Flow cytometry revealed that leptin stimulated transformation of U87-MG cells from G0/G1 phase to S phase,but had no effects on the cell apoptosis.STAT3 mRNA and protein expressions in U87-MG cells were significantly upregulated.The subcutaneous tumor model in nude mice showed that leptin significantly increased the growth of U87-MG xenografts and elevated STAT3 expression.Conclusion:Leptin can significantly increase the growth of human glioma,and its mechanism might be related to the activation of the JAK2-STAT3 signaling pathway.
出处 《肿瘤》 CAS CSCD 北大核心 2010年第9期735-739,共5页 Tumor
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  • 1赵声明,常乃柏,顾惜春.转导JAK2基因可促进原始多能造血细胞在体外的长期扩增[J].中华医学杂志,2004,84(11):949-953. 被引量:2
  • 2侯丽颖,贺松其,文彬,吕志平.保肝宁对瘦素刺激HSC增殖及其JAK_2-STAT_3信号通路影响的实验研究[J].上海中医药杂志,2007,41(3):60-62. 被引量:13
  • 3HOU S X, ZHENG Z, CHEN X, et al. The JAK/STAT pathway in model organisms: Emerging roles in cell movement[ J]. Developmental Cell, 2002, 3 (6) : 765 -778.
  • 4DALAL I, ARPAIA E, DADI H, et al. Cloning and characterization of the human homolog of mouse JAK2 [ J ]. Blood, 1998, 91(3) : 844 -851.
  • 5SALTZMAN A, STONE M, FRANKS C, et al. Cloning and characterization of human Jak-2 kinase: High mRNA expression in immune cells and muscle tissue [ J ].Biochemical and Biophysical Research Communications, 1998, 246(3):627-633.
  • 6NEUBAUER H, HUFFSTADT U, MULLER M, et al. Embryonic lethality in mice deficient in Janus kinase 2 (JAK2) [J]. Immunology Letters, 1997, 56: 275.
  • 7DUHE R J, RUI H, GREENWOOD J D, et al. Cloning of the gene encoding rat JAK2, a protein tyrosine kinase [J]. Gene, 1995, 158 (2) : 281 -285.
  • 8FRENZEL K, WALLACE T A, MCDOOM I, et al. A functional JAK2 tyrosine kinase domain is essential for mouse development [ J]. Experimental Cell Research, 2006, 312(15) : 2735 -2744.
  • 9RADOSEVIC N, WINTERSTEIN D, KELLER J R, et al. JAK2 contributes to the intrinsic capacity of primary hematopoietic cells to respond to stem cell factor [J].Experimental Hematology, 2004, 32 (2) : 149 - 156,.
  • 10MURAOKA O, XU B, TSURUMAKI T, et al. Leptin-induced transactivation of NPY gene promoter mediated by JAK1,JAK2 and STAT3 in the neural cell lines[J]. Neurochemistry International, 2003, 42 (7) : 591 - 601.

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