期刊文献+

急性淋巴细胞白血病患者 ASB2和 Jak3基因mRNA 表达的研究 被引量:3

Investigaion about the mRNA expression of ASB2 and Jak3 in patients with acute lymphoblastic leuke-mia
原文传递
导出
摘要 目的:研究急性淋巴细胞白血病(ALL)患者骨髓中锚蛋白重复序列和抑制细胞因子信号盒蛋白2(ASB2)和 Janus 激酶3(Jak3)mRNA 的表达及其两者的相关性。方法收集初诊的48例 ALL患者(37例 B 细胞 ALL,11例 T 细胞 ALL)和34例非白血病患者(对照组)骨髓,采用实时荧光定量 PCR检测骨髓中 ASB2和 Jak3 mRNA 表达情况。结果B 细胞 ALL 和 T 细胞 ALL 患者骨髓中 ASB2 mRNA表达量相对于对照组分别升高了32.7倍和68.5倍,差异均有统计学意义(t =20.1,P <0.01;t =23.1, P <0.01),Jak3 mRNA 表达量较对照组分别升高了2336.3和7131.5倍(t =70.2,P <0.01;t =90.4, P <0.01)。ASB2和 Jak3 mRNA 表达量具有相关性(r =0.523,P <0.001)。结论ASB2和 Jak3在 ALL患者骨髓中异常表达,且具有正相关性,两者可能共同参与白血病细胞的恶性增殖和异常分化。 Objective To explore the expression of ankyrin-repeat SOCS box containing protein 2 (ASB2)and Janus kinase 3 (Jak3)mRNA in bone marrow plasma mononuclear cells of patients with acute lymphoblastic leukemia (ALL)and discuss the correlation of them.Methods Bone marrow plasma was collected from 48 patients of newly diagnosed ALL (37 cases B-ALL and 11 cases T-ALL)and 34 non leukemia patients (control group),respectively.Expression levels of ASB2 and Jak3 mRNA were detected by real-time quantitative PCR.Results The expression of ASB2 mRNA in B-ALL and T-ALL were significantly different compared to control group (t =14.2,P 〈.01;t =15.2,P 〈.01),which were 68.5,32.7 folded more than control group,respectively.Moreover,the expression level of Jak3 mRNA in B-ALL group and T-ALL group were 2 336.1 and 7 131.5 folded more than control group (t =37.3,P 〈.01;t =37.6,P 〈.01). At last,the expression of ASB2 and Jak3 gene was positive correlation (r =0.523,P 〈.001).Conclusion ASB2 and Jak3 are expressed abnormally in ALL patients and the correlation of them is positive.ASB2 and Jak3 may be related to the proliferation and differentiation in leukemia cells.
出处 《国际肿瘤学杂志》 CAS 2016年第7期515-518,共4页 Journal of International Oncology
基金 国家自然科学基金(81200389)
关键词 白血病 淋巴样 骨髓 聚合酶链反应 锚蛋白重复序列和抑制细胞因子信号盒蛋白2 JANUS 激酶 3 Leukemia,lymphoid Bone marrow Polymerase chain reaction
  • 相关文献

参考文献17

  • 1Kohroki J, Nishiyama T, Nakamura T, et al. ASB proteins interact with Cullin5 and Rbx2 to form E3 ubiquitin ligase complexes [ J]. FEBS Lett, 2005, 579(30) : 6796-6802. 被引量:1
  • 2Heuze~ ML, Guibal FC, Banks C, et al. ASB2 is an Elongin BC-in- teracting protein that can assemble with Cullin 5 and Rbxl to reconsti- tute an E3 ubiquitin ligase complex [ J ]. J Biol Chem, 2005, 280 (7) : 5468-5474. 被引量:1
  • 3Kile BT, Metcalf D, Mifsud S, et al. Functional analysis of Asb-1 using genetic modification in mice[ J]. Mol Cell Biol, 2001,21 (18) : 6189-6197. 被引量:1
  • 4Chung AS, Guan YJ, Yuan ZL, et al. Ankyrin repeat and SOCS box 3( ASB3 ) mediates ubiquitination and degradation of tumor necrosis fac- tor receptor U [ J]. Mol Cell Biol, 2005,25 ( 11 ) : 4716-4726. 被引量:1
  • 5McDaneld TG, Spurlock DM. Ankyrin repeat and suppressor of cyto- kine signaling (SOCS) box-containing protein ( ASB ) 15 alters diffe- rentiation of mouse C2C12 myoblasts and phosphorylation of mitogen- activated protein kinase and Akt [ J ]. J Anita Sci, 2008, 86 ( 11 ) : 2897-2902. 被引量:1
  • 6王妍,徐酉华.糖原合成酶激酶3β与白血病[J].国际肿瘤学杂志,2013,40(5):373-376. 被引量:1
  • 7Taniguchi T. Cytokine signaling through nonreeeptor protein tyrosine kinases[J]. Science, 1995, 268(528): 251-255. 被引量:1
  • 8Wells JA, Devos AM. Hematopoietic receptor complexes [ J ]. Annu Rev Biochem, 1996, 65: 609-634. 被引量:1
  • 9Noguehi, Nakamura, Russell, et al. Interleukin-2 receptor gamma chain : a functional component of the interleukin-7 receptor [ J ]. Sci- ence, 1993, 262: 1877-1880. 被引量:1
  • 10Nosaka T, Van Deursen JM, Tripp RA, et al. Defective lymphoid development in mice lacking Jak3 [J]. Science, 1995, 270: 800- 802. 被引量:1

二级参考文献37

  • 1左明新,陈晓光.糖原合成酶激酶-3及其抑制剂研究进展[J].国际药学研究杂志,2007,34(4):259-262. 被引量:6
  • 2Phukan S, Babu VS, Kannoji A, et al. GSK3beta: role in therapeu- tic lartdscape and development of modulators. Br J Pharmacol, 2010, 160(1) :1-19. 被引量:1
  • 3Grumolato L, Liu G, Mong P, et al. Canonical and noncanonical Wnts use a common mechanism to activate completely unrelated core- ceptors. Genes Dev, 2010, 24(22) :2517-2530. 被引量:1
  • 4Abrahamsson AE, Geron I, Gotlib J, et al. Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation. Proc Natl Acad Sci USA, 2009, 106(10) :3925-3929. 被引量:1
  • 5Polak R, Buitenhuis M. The PI3K/PKB signaling module as key reg- ulator of hematopoiesis : implications for therapeutic strategies in leu- kemia. Blood, 2012, 119(4) :911-923. 被引量:1
  • 6Wang R, Xia L, Gabrilove J, et al. Downregulation of Mcl-1 through GSK-313 activation contributes to arsenic trioxide-induced apoptosis in acute myeloid leukemia ceils. Leukemia, 2013, 27(2) :315-324. 被引量:1
  • 7Huang WC, Lin YS, Chen CL, et al. Glycogen synthase kinase-3 beta mediates endoplasmic reticulum stress-induced lysosomal apoptosis in leukemia. J Pharmacol Exp Ther, 2009, 329(2) :524-531. 被引量:1
  • 8Sun SC, Cesarman E. NF-KB as a target for oncogenic viruses. Curt Top Microbiol Immunol, 2011,349 : 197-244. 被引量:1
  • 9Andrei VO, Nancy DB, Martin EF, et al. Inhibition of glycogen syn- thase kinase-3 activity leads to epigenetic silencing of nuclear factor kappaB target genes and induction of apoptosis in chronic lymphocytic leukemia B ceils. Blood, 2007, 110(2) :735-742. 被引量:1
  • 10Hu Y, Gu X, Li R, et al. Glycogen synthase kinase-3 inhibition induces nuclear factor-KB-mediated apoptosis in pediatric acute lym- phocyte leukemia cells. J Exp Clin Cancer Res, 2010, 29:154. 被引量:1

共引文献1

同被引文献25

引证文献3

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