期刊文献+

肝癌细胞BEL-7402中STAT3的组成性活性及对细胞迁移影响的研究 被引量:1

THE STUDY ON THE STAT3 LABELED BY GFP AFFECTING THE MIGRATION OF BEL-7402 CELL LINE
下载PDF
导出
摘要 信号转导和转录激活因子(STATs,Signaltransducersandactivatorsoftranscription)是JAK-STATs信号途径中一类重要的DNA结合蛋白,其异常表达和活化与多种肿瘤相关。本文研究发现,在肝癌细胞BEL-7402中STAT3具有组成性活性,能够持续地磷酸化,并转移入细胞核中行使功能。同时,我们成功构建了绿色荧光蛋白(GFP)标记的STAT3野生型(WT)/突变体(CYF)融合质粒,将其转入细胞,以荧光素酶报告系统验证了融合蛋白的活性;通过测定绿色荧光为标记的细胞迁移距离的方法证实,过表达野生型STAT3对肝癌细胞系BEL-7402细胞迁移有促进作用,而突变体STAT3能够降低癌细胞的迁移。 Signal transducers and activators of transcription (STATs) are key DNA-binding proteins in JAK/STATs signal pathway. Aberrant expression and activation of STAT3 have been identified in many kinds of tumors. We report here that constitutive activation of STAT3 was present in BEL-7402 cells. We constructed the fusing genes of STAT3 (wild type/mutant) and GFP to study the function of constitutively activated STAT3 in BEL-7402 cells. By measuring the migration of the cells labeled by GFP-STAT3(WT/CYF), we proved that overexpression of STAT3(WT) could augment the migration of BEL-7402 cells, while STAT3(CYF) could decrease the migration.
出处 《实验生物学报》 SCIE CAS CSCD 北大核心 2005年第4期317-323,共7页 Acta Biologiae Experimentalis Sinica
基金 江苏省科技项目资助(BK2000038)
关键词 肝癌细胞 BEL-7402 STAT3 组成性活性 细胞迁移 信号转导因子 转录激活因子 STAT3. GFP. BEL-7402. Constitutive Activation. Migration
  • 相关文献

参考文献14

  • 1Ihle, J.N., 1996, STATs: Signal transducers and activators of transcription. Cell, 84(3): 331-334.
  • 2Leonard, W. J., 2001, Role of Jak kinases and STATs in cytokine signal transduction. Int. J. Hemato., 73(3):271-277.
  • 3Decker, T., 1999, Introduction: STATs as essential intracellular mediators of cytokine responses. Cell. Mol.Life Sci., 55(12): 1505-1508.
  • 4Hoey, T. & M. J. Gmsby, 1999, STATs as mediators of cytokine-induced response. Adv. Immunol.,71: 145-162.
  • 5Takeda, K., K. Noguchi, W. Shi, T. Tanaka, M. Matsumoto, N. Yoshida, T. Kishimoto & S. Akira, 1997,Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality. Proc. Natl. Acad. Sci., 94(8):3801-3804.
  • 6Ni, Z., W. Lou, E. S. Leman & A.C. Gao, 2000, Inhibition of constitutively activated STAT3 signaling pathway suppresses growth of prostate cancer cells. Cancer Res., 60(5): 1225-1228.
  • 7Demoulin, J. B., E. Van Roost, M. Steven, B. Groner & J.C. Renauld, 1999, Distinct roles for STAT1,STAT3 and STAT5 in differentiation gene induction and apoptosis inhibition by interleukin-9. J. Biol.Chem., 274(36): 25855-25861.
  • 8Buettner, R., L. B. Mora & R. Jove, 2002, Activated STAT Signaling in human tumors provides novel molecular targets for therapeutic intervention. Clin, Cancer Res., 8(4): 945-954.
  • 9Kaptein, A., V. Paillard & M. Saunder, 1996, Dominant negative stat3 mutant inhibits IL-6-induced Jak-Stat signal mmsduction. J. Biol. Chem., 271(11): 5961-5964.
  • 10Niu, G., R. Heller, R. Catlett-Falcone, D. Coppola, M.Jaroszeski, W. Dalton, R. Jove & Yu H., 1999, Gene therapy with dominant -negative Stat3 suppresses growth of the murine melanoma B16 tumor in vivo. Cancer Res., 59(20):5059-5063.

同被引文献4

引证文献1

二级引证文献1

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