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MSI2在胰腺癌中的表达及其临床意义 被引量:3

Clinicopathological significance of MSI2 expression in human pancreatic cancer
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摘要 目的 检测胰腺导管腺癌(PDAC)组织中Musashi 2(MSI2)蛋白和mRNA的表达,分析癌组织MSI2表达与临床病理参数的相关性.方法 应用免疫组化方法检测61例PDAC组织及配对癌旁组织MSI2蛋白表达水平,采用蛋白质印迹法及实时PCR法检测10例癌组织及配对癌旁组织MSI2蛋白及mRNA的表达.分析癌组织MSI2表达与肿瘤临床病理参数的关系.结果 61例PADC患者癌组织MSI2高表达率为63.9%,配对癌旁组织为41.0%,癌组织的表达显著高于配对的癌旁组织,差异有统计学意义(t =2.809,P=0.007).10例癌组织及癌旁组织的MSI2蛋白表达量分别为0.748±0.195、0.420±0.171;癌组织MSI2 mRNA的表达量为癌旁组织表达量的(2.507±2.981)倍,差异均有统计学意义(t=3.689,P=0.005;t=2.660,P=0.026).癌组织MSI2表达仅与肿瘤大小呈正相关(x2=5.096,P =0.024),而与其他参数均无相关性.MSI2高表达患者的术后中位生存期为321 d,低表达者为730 d,高表达者的生存期显著短于低表达者,差异有统计学意义(x2=6.706,P=0.010).结论 胰腺癌组织中MSI2表达上调,其表达量与肿瘤大小相关,高表达患者的预后差. Objective To detect the expression of MSI2 protein and mRNA in pancreatic ductal adenocarcinoma (PDAC) tissue,and investigate the correlation between the expression of MSI2 protein and the clinicopathological parameters.Methods The expression of MSI2 protein in 61 PDAC specimens and paired adjacent non-cancerous pancreatic tissues were detected by immunohistochemistry.Western blot and quantitative real-time PCR (QRT-PCR) were used to examine the expression of MSI2 protein and mRNA level in 10 PDAC specimens and adjacent non-cancerous pancreatic tissues.Then the relationship between MSI2 expression in cancerous tissues and clinicopathological parameters was analyzed.Results In 61 patients with PDAC,the expression rate of MSI2 protein was higher in cancerous tissues (63.9%) compared with that in paired non-cancerous pancreatic tissues (41.0%),and the difference between the two groups was statistically significant (t =2.809,P =0.007).The expression levels of MSI2 protein in 10 fresh PDAC specimens and adjacent non-cancerous pancreatic tissues were 0.748 ± 0.195 and 0.420 ± 0.171,and the expression level of MSI2 mRNA in PDAC specimens was as 2.507 ± 2.981 times as much of adjacent non-cancerous pancreatic tissues,and the difference between the two groups was statistically significant (t =3.689,P=0.005;t =2.660,P =0.026).The expression of MSI2 in cancerous tissues was only positively associated with the size of the tumor (x2 =5.096,P =0.024),but it was not associated with other parameters.The median survival of patients with high MSI2 expression was 321 d,and it was 730 d for patients with low MSI2 expression,and the median survival of patients with high MSI2 expression was significantly shorter than that of low MSI2 expression (x2 =6.706,P =0.010).Conclusions The expression MSI2 is up-regulated in PDAC and related to the tumor size.The patients with high expression of MSI2 protein have poor prognosis.
出处 《中华胰腺病杂志》 CAS 2014年第6期392-395,共4页 Chinese Journal of Pancreatology
基金 沈阳市科学技术计划项目(F11-264-1-09) 辽宁省高等学校优秀科技人才支持计划(LR2011023) 辽宁省科学技术计划项目(2011225019)
关键词 胰腺肿瘤 基因表达 Musashi2 病理学 临床 预后 Pancreatic neoplasms Gene expression Pathology,clinical
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  • 1Jemal A, Siegel R, Ward E, et al. Canc, er statistics, 2009 [ J]. CA Cancer J Clin, 2009,59 (4) :225-249.
  • 2Thol F, Winschel C, Sonntag AK, et al. Prognostic significance of expression levels of stem cell regulators MSI2 and NUMB in acute myeloid leukemia [ J ]. Ann Hematol, 2013,92 ( 3 ) : 315- 323.
  • 3Kharas MG, Lengner C J, AI-Shahrour F,et al. Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia [J]. Nat Med, 2010,16(8): 903-908.
  • 4He L, Zhou X, Qu c, et al. Musashi2 predicts poor prognosis and invasion in hepatocellular carcinoma by driving epithelial- mesenchymal transition[J]. J Cell Mol Med, 2014,18(1):49- 58.
  • 5Emadi-Baygi M, Nikpour P, Mohammad-Hashem F,et al. MSI2 expl~ssion is decreased in grade H of gastric carcinoma [ J ]. Pathol Res Pract, 2013,209( 11 ) : 689,-691.
  • 6Supuran CT, Carbonic anhydrase inhibitors and activators for novel therapeutic applications [ J ]. Future Med Chem, 2011,3 (9) :1165-1180.
  • 7Mu Q, Wang Y, Chen B, et al. High expression of Musashi-2 indicates poor prognosis in adult B-cell acute lymphohlastic leukemia [ J ]. Leuk Res, 2013,37 ( 8 ) :922-927.
  • 8Ito T, Kwon HY, Zimdahl B, et al. Regulation of myeloid leukaemia by the cell-fate determinant Musashi [ J ]. Nature, 2010,466 ( 7307 ) : 765-768.
  • 9Griner LN, Reuther GW. Aggressive myeloid leukemia formation is directed by the Musashi2/Numb pathway [ J ]. Cancer Biol Ther, 2010,10(10) :979-982.
  • 10邹秀平,黄伟,刘珊珊,徐艳玲.MSI2和Numb在白血病中的表达及分析[J].临床血液学杂志,2013,26(3):319-321. 被引量:2

二级参考文献40

  • 1ITO T,KWON H Y,ZIMDAHL B,et al. Regulationof myeloid leukaemia by the cell-fate determinant Mu-sashi[J]. Nature,2010,466 : 765 — 768.
  • 2NAKAMURA M,OKANO H,BLENDY J A,et al.Musashi, a neural RNA-binding protein required forDrosophila adult external sensory organ development[J]. Neuron, 1994,13 :67 — 81.
  • 3IMAI T, TOKUNAGA A,YOSHIDA T, et al. Theneural RNA-binding protein Musashi-1 translationallyregulates the m-numb gene expression byinteractingwith its mRNA[J]. Mol Cell Biol, 2001, 21 : 3888 —3900.
  • 4OKANO H,KAWAHARA H,TORIYA M. Functionof RNA-binding protein Musashi-1 in stem cells[J].Exp Cell Res,2005,306 :349 — 356.
  • 5BARBOUTI A, HOGLUND M, JOHANSSON B,etal. A novel gene,MSI2,encoding a putative RNA-binding protein is recurrently rearranged at diseaseprogression of chronic myeloid leukemia and forms afusion gene with HOXA9 as a result of the cryptic t(7 ; 17) (pl5;q23) [J]. Cancer Res, 2003 , 63 . 1202 —1206.
  • 6KHARAS M G,LENGNER C J,AL-SHAHROURF,et al. Musashi-2 regulates normal hematopoiesis andpromotes aggressive myeloid leukemia [J]. Nat Med,2010,16:903-908.
  • 7BYERS R J, CURRIE T,THOLOULI E,et al. MSI2protein expression predicts unfavorable outcome in a-cute myeloid leukemia [J]. Blood, 2011, 118: 2857 —2867.
  • 8LIVAK K J,SCHMITTGEN T D. Analysis of relativegene expression data using real-time quantitative PCRand the 2(-Delta Delta C(T)) Method[J]. Methods,2001,25:402-408.
  • 9SCHMITTGEN T D,LIVAK K J. Analyzing real-timePCR data by the comparative C(T) method[J]. NatProtoc,2008,3:1101-1108.
  • 10KANEMURA Y,MORI K,SAKAKIBARA S,et al.Musashil,an evolutionarily conserved neural RNA-binding protein,is a versatile marker of human gliomacells in determining their cellular origin, malignancy,and proliferative activity[J]. Differentiation, 2001, 68 ;141-152.

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