期刊文献+

microRNA-219-2-3p在胃癌中的表达及其作用机制初探 被引量:5

The role of microRNA-219-2-3p in Gastric Cancer and the underlying mechanism
在线阅读 下载PDF
导出
摘要 目的探讨microRNA-219-2-3p(miR-219-2-3p)与胃癌的相关性及机制。方法运用实时聚合酶链反应(real timeRT PCR)检测82份配对的胃癌组织和周围正常组织样本中的miR-219-2-3p的表达水平。在胃癌细胞株MGC803中过表达miR-219-2-3p后,测定细胞增殖活性,并在细胞株和胃癌组织标本中采用蛋白免疫印迹法(Western blot)测定与肿瘤增殖相关的蛋白ERK1/2表达水平。结果 miR-219-2-3p在晚期胃癌组织中的表达量下降,差异有统计学意义(P<0.05)。在胃癌细胞株MGC803中过表达miR-219-2-3p后细胞增殖受显著抑制(P<0.05)。过表达miR-219-2-3p后,MGC803细胞中的ERK磷酸化水平显著下降,总ERK表达量不变。在组织标本中,胃癌组织的ERK磷酸化(p-ERK)水平明显高于周围癌旁组织。结论 miR-219-2-3p可能通过参与调控ERK1/2信号通路而在胃癌发生和发展中起抑癌基因的作用。 Objective To evaluate the role of miR219‐2‐3p in gastric cancer and the underlying mechanisms .Methods Real time RT‐PCR was employed to quantify the expression level of miR219‐2‐3p in matched tissues of 82 patients .In vitro cell proliferation , the expression of tumorgenesis related protein ERK1/2 was performed by overexpressing miR‐219‐2‐3p in gastric cancer cell line MGC803 .Results The expression level of miR‐219‐2‐3p significantly decreased in late stage gastric cancer (P〈 0 .05) .The cell proliferation rate was significantly reduced in gastric cancer cell lines overexpressing miR‐219‐2‐3p .Furthermore ,the expression level of p‐ERK that activated form of ERK was significantly decreased whereas the total level of ERK was unchanged after overex‐pressing of miR‐219‐2‐3p in MGC803 cell lines .The expression level of p‐ERK was also increased in gastric cancer tissues .Conclu‐sion miR‐219‐2‐3p may acts as a tumor suppressor in gastric cancer by decreasing the activity of ERK 1/2 signaling pathway .
出处 《重庆医学》 CAS CSCD 北大核心 2014年第14期1729-1731,共3页 Chongqing medicine
关键词 胃肿瘤 microRNA-219-2-3p 细胞分裂 stomach neoplasms microRNA-219-2-3p cell division
  • 相关文献

参考文献2

二级参考文献14

共引文献208

同被引文献21

  • 1李永军,徐兆强,王德杭,卢凯华.^(99)Tc^m-HL91显像、CT和血清肿瘤标志物测定联合应用诊断肺癌[J].中华核医学杂志,2005,25(2):93-95. 被引量:5
  • 2Tefferi A, Pardanani A, Lim KH, et al. TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis[J]. Leukemia, 2009, 23(5) :905-911.
  • 3Makishima H, Jankowska AM, McDevitt MA, et al. CBL, CBLB,TET2, ASXL1, and IDH1/2 mutations and addi- tional chromosomal aberrations constitute molecular e- vents in chronic myelogenous leukemia[J]. Blood, 2011, 117(21) : e198-206.
  • 4Jardin F, Ruminy P, Parmentier F, et al. TET2 and TP53mutations are frequently observed in blastic plasmacytoid dendritic cell neoplasm[J]. Br J Haematol, 2011,153 (3) : 413-416.
  • 5Yang H ,Liu Y,Bai F,et al. Tumor development is associ- ated with decrease of TET gene expression and 5-methyl- cytosine hydroxyIation[J]. Oncogene, 2013,32 (5) : 663- 669.
  • 6Suzuki MM, Bird A. DNA methylation landscapes: pro- vocative insights from epigenomics[J]. Nat Rev Genet, 2008,9 (6) : 465-476.
  • 7Loenarz C,Schofield CJ. Oxygenase catalyzed 5-methylcy- tosine hydroxylation [J ]. Chem Biol, 2009, 16 (6) : 580- 583.
  • 8He YF, Li BZ, Li Z, et al. Tet-mediated formation of 5- carboxylcytosine and its excision by TDG in mammalian DNA[J]. Science, 2011,333(6047) : 1303-1307.
  • 9Su JS, Laura P, Min SS, et al. MicroRNA-antagonism reg- ulates breast cancer stemness an metastasis via TET fam- ily dependent chromatin remodeling [J]. Cell, 2013, 154 (2) :311-324.
  • 10Mancini M,Veljkovic N,Leo E, et al. Cytoplasmatic com- partmentalization by Brc-Abl promotes TET2 loss-of- function in chronic myeloid leukemia[J]. J Cell Biochem, 2012,113 (8) : 2765-2774.

引证文献5

二级引证文献19

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