中文摘要：

瞄准：阐明在人的胰腺的癌症细胞生长的 dickkopf3 (Dkk3 ) 的角色。方法：在人的胰腺的癌症房间线的 Dkk3 mRNA 和蛋白质表示被即时反向的抄写聚合酶链反应(即时 RT-PCR ) 检测，西方的弄污和 immunofluorescence。Dkk3 倡导者顺序的 Methylation 被 methylation 特定的聚合酶链反应(MSP ) 检验， Dkk3 mRNA 表示被即时 RT-PCR 在 5-aza-2-deoxycytidine (5-aza-dC ) 以后决定治疗。癌症房间增长上并且在到 gemcitabine 的 vitro 敏感的 Dkk3 的效果被 CellTiter 96 调查吗？水的在 transfecting 以后的答案房间增长试金(山) Dkk3 表示 plasmid 进人的胰腺的癌症房间。细胞外的调整信号的蛋白质 kinases (津贴) 和细胞外的调整信号的蛋白质 kinases (英皇家空军之阶级最低之兵) 也是的 -catenin, phosphorylated 的表示由即时 RT-PCR 并且在人的胰腺的癌症房间的在 upregulating Dkk3 表示以后的西方的弄污检验了。结果：结果证明 Dkk3 mRNA 和蛋白质的表示层次在测试的所有胰腺的癌症房间线是低的。Dkk3 倡导者顺序是在 MIA PaCa-2 和 AsPC-1 房间线的 methylated，它显示出减少的 Dkk3 表示。这二根房间线，开始有一个 methylated Dkk3 倡导者，显示出依赖于剂量并且 DNA demethylating 代理人预定的增加的 Dkk3 mRNA 表示， 5-aza-dC，治疗(P < 0.05 或 P < 0.01 ) 。当 Dkk3 表示是跟随 Dkk3 表示 plasmid 的 transfection 进 MIA PaCa-2 房间的 upregulated 时，房间的能力减少了增殖(P < 0.01 ) ，并且 -catenin 和津贴的表示是 downregulated (P < 0.01 ) 。到 gemcitabine 的敏感在 Dkk3 表示 plasmid-transfected 房间被提高。结论：我们的调查结果第一次，含有 Dkk3 作为在人的胰腺的癌症的肿瘤 suppressor，通过经由调停英皇家空军之阶级最低之兵的小径的 -catenin 表示的 downregulation。

英文摘要：

AIM：To elucidate the role of dickkopf3（Dkk3）in human pancreatic cancer cell growth.METHODS：Dkk3 mRNA and protein expression in human pancreatic cancer cell lines were detected by realtime reverse transcription polymerase chain reaction（realtime RTPCR）,Western blotting and immunofluorescence.Methylation of the Dkk3 promoter sequence was examined by methylationspecific polymerase chain reaction（MSP）and Dkk3 mRNA expression was determined by realtime RTPCR after 5aza2＇deoxycytidine（5azadC）treatment.The effects of Dkk3 on cancer cell proliferation and in vitro sensitivity to gemcitabine were investigated by CellTiter 96？AQueous One Solution Cell Proliferation Assay（MTS）after transfecting the Dkk3 expression plasmid into human pancreatic cancer cells.The expression ofβcatenin,phosphorylated extracellular signalregulated protein kinases（pERK）and extracellular signalregulated protein kinases（ERK）was also examined by realtime RTPCR and Western blotting after upregulating Dkk3 expression in human pancreatic cancer cells.RESULTS：The results show that the expression levels of both Dkk3 mRNA and protein were low in all pancreatic cancer cell lines tested.The Dkk3 promoter sequence was methylated in the MIA PaCa2 and AsPC1 cell lines,which showed reduced Dkk3 expression.These two cell lines,which initially had a methylated Dkk3 promoter,showed increased Dkk3 mRNA expression that was dependent upon the dosage and timing of the DNA demethylating agent,5azadC,treatment（P0.05 or P0.01）.When Dkk3 expression was upregulated following the transfection of a Dkk3 expression plasmid into MIA PaCa2 cells,the ability of cells to proliferate decreased（P0.01）,and the expression ofβcatenin and pERK was downregulated（P0.01）.Sensitivity to gemcitabine was enhanced in Dkk3 expression plasmidtransfected cells.CONCLUSION：Our findings,for the first time,implicate Dkk3 as a tumor suppressor in human pancreatic cancer,through the downregulation ofβcatenin expression via the ERKmediated pathway.