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JAK家族基因与细胞因子信号传导抑制因子家族基因在白血病细胞中的表达及意义

The clinical significance and the expression of JAKs and suppressor of cytokine signaling genes in leukemia cells
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摘要 目的探讨SOCSs基因和JAKs基因在急性髓系白血病(AML)患者中的表达情况。方法RT-PCR方法检测AML患者和正常对照骨髓SOCS1~7、JAK1~3和TYK 2mRNA的表达。结果①AML患者SOCS1、4、5、7的表达明显低于缓解组和正常对照组(P〈0.01),SOCS3、6表达水平较缓解组和正常对照组高(P〈0.01),SOCS2在各组无明显差异;AML患者JAK2、JAK3、TYK2 mRNA平均表达水平较缓解组和正常对照组明显增高(P〈0.05)。初治AML患者JAKl mRNA表达水平较正常对照组略增高,但差异无统计学意义(P〉0.05),复发AML患者JAKl mRNA表达水平较正常对照组明显增高(P〈0.05)。结论AML患者的SOCS1、4、5、7基因表达缺失或降低,JAK家族基因表达明显增高,提示二者可能共同参与髓系白血病的发生。 Objective To investigate the expression of suppressor of cytokine signaling genes ( SOCSs ) and JAKs mRNA in the acute myloid leukemia(AML) patients. Methods The expression of SOCSs and JAKs mRNA as well as TYK2 in AML patients and healthy adults as normal contrals ( NC ) was measured with RT-PCR. Results The expression of SOCS 1,4,5 and 7 in AML patients was lower than those in normal control and AML with remission ( P 〈 0.01 ) , but the expression of SOCS 3 and 6 was higher than those in normal control and remission AML( P 〈 0.01 ) , however there was no significant difference in SOC2 between groups. The expressions of JAK2, JAK3 and TYK2 in AML were significantly higher than those in patients with remission and normal control ( P 〈 0.05 ). The expression of JAK1 mRNA in relapsed AML was higher than that in normal control group ( P 〈 0.05 ) , but the latter has no statistical significance between beginning treatment and normal group(P 〉 0.05). Conclusion The deletion and degradion of SOCS 1,4,5 and 7 present in AML patients and JAKs expression is significantly increased, suggesting that both of them may co-participate in the pathogenesis of AML.
出处 《中国综合临床》 北大核心 2008年第12期1196-1199,共4页 Clinical Medicine of China
基金 河北省自然科学基金项目(C2005000744)
关键词 白血病 SOCSs基因 JAKs基因 Leukemia Suppressor of cytokine signaling genes JAKs
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参考文献11

  • 1Biethahn S, Alves F, Wilde S, et al. Expression of granulocyte colo- ny-stimulating factor- and granulocyte-macrophage colony-stimulating factor-associated signal transduction proteins of the JAK/STAT pathway in normal granulopoiesis and in blast cells of acute myelogenous leukemia [ J ]. Exp Hematol, 1999,27 ( 5 ) : 885 -894.
  • 2Jiao H, Berrada K, Yang W, et al. Direct association with and dephosphorylation of JAK2 kinase by the SH2-domain-containing protein tyrosine phosphatase SHP-1 [ J]. Mol Cell Biol, 1996,16 (12) : 6985-6992.
  • 3李英华,罗建民,张晓燕,王冬梅.SHP-1和JAK1基因在初治急性白血病患者中的表达[J].国际病理科学与临床杂志,2007,27(4):284-287. 被引量:2
  • 4魏秀青,余平,黎明.细胞因子信号转导抑制分子的研究进展[J].国外医学(生理病理科学与临床分册),2005,25(1):14-17. 被引量:8
  • 5Wu C, Guan Q, Wang Y, et al. SHP-1 suppresses cancer cell growth by promating degradation of JAK kinase[ J]. J Cell Biochem,2003, 90(5) :1026-1037.
  • 6Han Y, Amin H, Franko B, et al. Loss of SHP1 enhances JAK3/ STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK-positive anaplastic large-cell lymphoma [ J ]. Blood ,2006,108 ( 8 ) : 2796-2803.
  • 7Matsumoto A, Masuhara M, Mitsui K, et al. CIS, a cytokine SH2 - protein, is a target of the Jak - STAr5 pathway and modulates STATS activation[ J]. Blood, 1997,89 (9) :3148-3154.
  • 8Verdier F, Chretien S, Muller O, et al. Proteasomes regulate erythropoietin receptor and signal transducer and activator of transcription 5 ( STAT5 ) activation [ J ]. J Biol Chem, 1998,273 ( 43 ) : 28185- 28190.
  • 9Liu TC, Lin SF, Chang JG, et al. Epigenetic alteration of the SOCS1 gene in chronic myeloid leukemia [ J ]. Br J Haematol, 2003,123 (4) :654-661.
  • 10Chen CY,T say W,Tang JL, et al. SOCS1 methylation in patients with newly diagnosed acute myeloid leukemia [ J ]. Genes Chromo- Somes Cancer,2003,37 ( 3 ) :300-305.

二级参考文献31

  • 1韩颖,罗建民,贾晓辉,王福旭,姚丽,杜行严.白血病患者造血细胞磷酸酶与半胱氨酸蛋白酶基因表达及其临床意义[J].中华内科杂志,2006,45(5):363-365. 被引量:18
  • 2李英华,罗建民.白血病形成中JAK/STAT信号通路的持续激活[J].国际病理科学与临床杂志,2006,26(5):398-402. 被引量:6
  • 3Zhang JG, Metealf D, Rakar S, et al. The SOCS box of suppressor of cytokine signaling-1 is important for inhibition of cytokine action in vivo[J]. Proc Natl Acad Sci USA, 2001,98(23) :13261-13265.
  • 4Saito H, Morita T, Fujimoto N, et al. IFN regulatory factor-1-mediated transcriptional activation of mouse STAT inhibitor -1 gene promoter by IFN-gamma [J]. J Immunol, 2000, 164 ( 11 ) : 5833-5843.
  • 5Emanuelli B, Peraldi P, Filloux C, et al. SOCS-3 is an insulin-induced negative regulator of insulin signaling [ J ]. J Biol Chem,2000, 275(21 ) :15985-15991.
  • 6Gregorieff A, Pyronnet S, Sonenberg N, et al. Regulation of SOCS-1 expression by translational repression [ J ]. J Biol Chem, 2000,275 (28) :21596-21604.
  • 7Cornish AL, Chong MM, Davey GM, et al. SOCS-1 regulates signaling in response to IL-2 and other gamma c-dependent cytokines in peripheral T cells [ J ]. J Biol Chem, 2003, 278 ( 25 ) : 22755-22761.
  • 8Nakagawa R, Naka T, Tsutsui H, et al. SOCS-1 participates in negative regulation of LPS responses[J]. Immunity, 21302, 17(5) :677-687.
  • 9Yoshikawa H, Matsubara K, Qian GS, et al. SOCS-1, a negative regulator of the JAK/STAT pathway, is silenced by methylation in human hepatocellular carcinoma and shows growth-suppression activity[J]. Nat Genet, 2001 ,28(1 ) :29-35.
  • 10Metcalf D, Mifsud S, Di Rago L, et al. Polycystic kidneys and chronic inflammatory lesions are the delayed consequences of loss of the suppressor of cytokine signaling-1 ( SOCS-1 ) [ J ]. Proc Natl Acad Sci USA, 2002, 99(2) :943-948.

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