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SOCS3基因转染对肺腺癌细胞株A549原癌基因c-fos、c-jun mRNA表达及细胞增殖的影响 被引量:5

Effects of transfected SOCS3 gene on expression of c-fos and c-jun mRNA and proliferation of A549 cells
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摘要 目的 探讨SOCS3基因对人肺腺癌细胞株A5 49中c fos、c junmRNA表达及细胞增殖的影响。方法 以脂质体为载体将pEFSOCS3和pSV2neo共转染至人肺腺癌细胞株A5 49,RT PCR和免疫细胞化学法测定转染前后细胞中SOCS3mRNA和蛋白表达 ;半定量RT PCR测定转染前后细胞中c fos、c junmRNA水平表达变化 ;3H TdR掺入法检测基因转染前后细胞增殖情况。结果 RT PCR和免疫细胞化学证实转染后细胞中有SOCS3稳定表达 ;半定量RT PCR证实转染后细胞中c fos、c junmRNA水平显著降低 (P <0 .0 1) ;且转染组细胞 3H TdR掺入量显著降低 (P <0 .0 1)。结论 SOCS3蛋白可能通过负性调控STAT3介导的信号通路降低c fos、c jun的表达 ,从而抑制肺癌细胞增殖。 Objective To explore the effects of transfected SOCS3 gene on the expression of c fos and c jun mRNA and proliferation of A549 cells. Methods A549 cells were cotransfected with pEFSOCS3 and pSV2neo by liposome. Expressions of SOCS3 mRNA and protein were detected by RT PCR and immunocytochemical method, respectively. The expression of c fos and c jun mRNA was assessed by semi quantitative RT PCR. 3H TdR incorporation was used to measure the cell proliferation. Results The SOCS3 expression in A549 cells transfected with SOCS3 gene was confirmed by RT PCR and immunocytochemical method, respectively. Compared with that in the control group, c fos and c jun mRNA level decreased significantly in pEFSOCS3 transfected A549 cells ( P <0 01). 3H TdR incorporation in pEFSOCS3 transfected A549 cells was significantly lower than that in the control group ( P <0.01). Conclusion SOCS3 protein might decrease the expression of c fos and c jun and inhibit the proliferation of A549 cells by regulating STAT3 mediated signal pathway negatively.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2004年第17期1549-1552,共4页 Journal of Third Military Medical University
关键词 SOCS3 C-FOS C-JUN 肺腺癌 增殖 SOCS3 c fos c jun lung adenocarcinoma proliferation
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  • 1Boudny V, Kovarik J. JAK/STAT signaling pathways and cancer. Janus kinases/signal transducers and activators of transcription [ J ]. Neoplasma,2002, 49(6): 349 - 355.
  • 2Starr R, Willson T A, Viney E M, et al. A family of cytokine-inducible inhibitors of signalling[J]. Nature, 1997, 387(6636): 917-921.
  • 3Levy D E, Lee C K. What does Stat3 do[J]? J Clin Invest, 2002, 109(9): 1143- 1148.
  • 4Bromberg J. Stat proteins and oncogenesis[J]. J Clin Invest, 2002, 109(9): 1139- 1142.
  • 5Mora L B, Buettner R, Seigne J, et al. Constitutive activation of Stat3 in human prostate tumors and cell lines: direct inhibition of Stat3 signaling induces apoptosis of prostate cancer cells[J]. Cancer Res, 2002, 62 (22):6659 - 6666.
  • 6Schuringa J J, Wierenga A T, Kruijer W, et al. Constitutive Stat3,Tyr705, and Ser727 phosphorylation in acute myeloid leukemia cells caused by the autocrine secretion of interleukin-6[J]. Blood, 2000, 95(12): 3765 -3770.
  • 7Brender C, Nielsen M, Kaltoft K, et al. STAT3-mediated constitutive expression of SOCS-3 in cutaneous T-cell lymphoma[J]. Blood, 2001, 97(4): 1056- 1062.
  • 8Auernhammer C J, Bonsquet C, Melmed S. Autoregulation of pituitary corticotroph SOCS-3 expression: characterization of the murine SOCS-3 promoter[J]. Proc Natl Acad Sci USA, 1999, 96(12): 6964-6969.
  • 9Jochum W, Passegue E, Wagner E F. AP-1 in mouse development and tumorigenesis[J]. Oncogene, 2001, 20(19): 2401-2412.
  • 10Ivanov V N, Bhoumik A, Krasilnikov M, et al. Cooperation between STAT3 and c-jun suppresses Fas transcription [ J ]. Mol Cell, 2001, 7(3): 517-528.

二级参考文献16

  • 1Endo TA et al. Nature,1997, 387:921-924
  • 2Yasukawa H et al. EMBO J, 1999, 18:1309-1320
  • 3Verdier F et al. J Biol Chem, 1998, 273:28185-28190
  • 4Zhang JG et al. Proc Natl Acad Sci USA, 1999, 96:2071-2076
  • 5Marine JC et al. 1999, 98:609-616
  • 6Naka T et al. Proc Natl Acad Sci USA, 1998, 95:15577-15582
  • 7Starr R et al. Proc Natl Acad Sci USA, 1998, 95:14395-14399
  • 8Metcalf D et al. Nature, 2000, 405:1069-1073
  • 9Sasaki A et al. J Bio Chem, 2000, 275:299338-299347
  • 10Starr R et al. Nature, 1997, 387(6636):917-921

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