期刊文献+

Effects of CPG ODN on biological behavior of PANC-1 and expression of TLR9 in pancreatic cancer 被引量:10

Effects of CPG ODN on biological behavior of PANC-1 and expression of TLR9 in pancreatic cancer
在线阅读 下载PDF
导出
摘要 AIM:To determine the expression of toll-like receptor 9(TLR9) in pancreatic tumor and the effects of cytosine phosphate-guanosine oligodeoxynucleotides 2216(CPG ODN2216) on biological behavior of pancreatic carcinoma cell line PANC-1 and explore their clinical significance.METHODS:The immunohistochemistry and Western blot were used to determine the expression of TLR9 protein in pancreatic cancer tissues,and immunofluorescence staining was performed to detect the TLR9 protein expression in pancreatic carcinoma cell line PANC-1.To assess the effects of CPG ODN2216 on the invasive property of Panc-1 cells,in vitro cell adhesion,wound-healing scrape,and invasion and cell colony formation were evaluated.RESULTS:TLR9 was highly expressed in pancreaticcancer tissues and PANC-1 cells.The percentage of positive cells expressing TLR9 protein in human pancreatic tissues,paracancerous tissues and normal tissues were 73.3%,33.3% and 20.0%,respectively,and the protein expression level of TLR9 was gradually descending(P < 0.05).In vitro tests in wound-healing scrape,cell adhesion,colony formation and matrigel invasion showed that the adhesion and motility of PANC-1 cells in CPG ODN 2216 treatment group were signif icantly lower than in the control group(P < 0.05).The cell growth assay showed that the proliferative ability of PANC-1 cells in treatment group was significantly decreased and CPG ODN2216 had an inhibitive effect in the growth of Panc-1 cells in a dose and time-dependent manner(P < 0.05).CONCLUSION:The gene of TLR9 is correlated with the invasive and metastatic potential of human pancreatic carcinoma,and CPG ODN2216 induces the inhibition of migration and invasion of Panc-1 cells. AIM:To determine the expression of toll-like receptor 9(TLR9) in pancreatic tumor and the effects of cytosine phosphate-guanosine oligodeoxynucleotides 2216(CPG ODN2216) on biological behavior of pancreatic carcinoma cell line PANC-1 and explore their clinical significance.METHODS:The immunohistochemistry and Western blot were used to determine the expression of TLR9 protein in pancreatic cancer tissues,and immunofluorescence staining was performed to detect the TLR9 protein expression in pancreatic carcinoma cell line PANC-1.To assess the effects of CPG ODN2216 on the invasive property of Panc-1 cells,in vitro cell adhesion,wound-healing scrape,and invasion and cell colony formation were evaluated.RESULTS:TLR9 was highly expressed in pancreaticcancer tissues and PANC-1 cells.The percentage of positive cells expressing TLR9 protein in human pancreatic tissues,paracancerous tissues and normal tissues were 73.3%,33.3% and 20.0%,respectively,and the protein expression level of TLR9 was gradually descending(P 〈 0.05).In vitro tests in wound-healing scrape,cell adhesion,colony formation and matrigel invasion showed that the adhesion and motility of PANC-1 cells in CPG ODN 2216 treatment group were signif icantly lower than in the control group(P 〈 0.05).The cell growth assay showed that the proliferative ability of PANC-1 cells in treatment group was significantly decreased and CPG ODN2216 had an inhibitive effect in the growth of Panc-1 cells in a dose and time-dependent manner(P 〈 0.05).CONCLUSION:The gene of TLR9 is correlated with the invasive and metastatic potential of human pancreatic carcinoma,and CPG ODN2216 induces the inhibition of migration and invasion of Panc-1 cells.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第8期996-1003,共8页 世界胃肠病学杂志(英文版)
基金 Supported by The National Natural Science Foundation of China, No. 30972898
关键词 Cytosine phosphate-guanosine oligodeoxynucleotides 2216 Pancreatic cancer Toll-like receptor 9 Biological behavior TLR9 生物学行为 寡核苷酸 胰腺癌 CpG 蛋白质表达 Toll样受体 人民政府
  • 相关文献

参考文献27

  • 1Jemal A, Siegel R, Ward E, Murray T, Xu J, Thun MJ. Cancer statistics, 2007. CA Cancer J Clin 2007; 57:43-66.
  • 2Hawes RH, Xiong Q, Waxman I, Chang KJ, Evans DB, Abbruzzese JL. A multispecialty approach to the diagnosis and management of pancreatic cancer. Am J Gastroenterol 2000; 95:17-31.
  • 3Real FX, Cibrian-Uhalte E, Martinelli P. Pancreatic cancer development and progression: remodeling the model. Gastroenterology 2008; 135:724-728.
  • 4Tanase CP, Dima S, Mihai M, Raducan E, Nicolescu MI, Albulescu L, Voiculescu B, Dumitrascu T, Cruceru LM, Leabu M, Popescu I, Hinescu ME. Caveolin-1 overexpression correlates with tumour progression markers in pancreatic ductal adenocarcinoma. J Mol Histo12009; 40:23-29.
  • 5Neoptolemos JP, Dunn JA, Stocken DD, Almond J, Link K, Beger H, Bassi C, Falconi M, Pederzoli P, Dervenis C, Fernandez-Cruz L, Lacaine F, Pap A, Spooner D, Kerr DJ, Friess H, Bflchler MW, Adjuvant chemoradiotherapy and chemotherapy in resectable pancreatic cancer: a randomised controlled trial. Lancet 2001; 358:1576-1585.
  • 6Jungert K, Buck A, von Wichert G, Adler G, Konig A, Buchholz M, Gress TM, Ellenrieder V. Spl is required for transforming growth factor-beta-induced mesenchymal transition and migration in pancreatic cancer cells. Cancer Res 2007; 67:1563-1570.
  • 7Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell 2006; 124:783-801.
  • 8O'Neill LA. How Toll-like receptors signal: what we know and what we don't know. Curr Opin Immunol2006; 18:3-9.
  • 9Cook DN, Pisetsky DS, Schwartz DA. Toll-like receptors in the pathogenesis of human disease. Nat Immunol 2004; 5: 975-979.
  • 10Goto Y, Arigami T, Kitago M, Nguyen SL, Narita N, Fertone S, Morton DL, Irie RF, Hoon DS. Activation of Toll- like receptors 2, 3, and 4 on human melanoma cells induces inflammatory factors. Mol Cancer Ther 2008; 7:3642-3653.

同被引文献25

  • 1王临虹,邱琇,郑睿敏,狄江丽.我国宫颈癌流行病学状况及防治策略的回顾与展望[J].中国妇幼卫生杂志,2010,1(3):146-149. 被引量:76
  • 2Juan Vaz,Hamid Akbarshahi,Roland Andersson.Controversial role of toll-like receptors in acute pancreatitis[J].World Journal of Gastroenterology,2013,19(5):616-630. 被引量:17
  • 3Rebecca Siegel,Deepa Naishadham,Ahmedin Jemal.Cancer statistics, 2013[J]. CA: A Cancer Journal for Clinicians . 2013 (1)
  • 4Lei Zheng,Jing Xue,Elizabeth M. Jaffee,Aida Habtezion.Role of Immune Cells and Immune-Based Therapies in Pancreatitis and Pancreatic Ductal Adenocarcinoma[J].Gastroenterology.2013(6)
  • 5Minoti V. Apte,Jeremy S. Wilson,Aurelia Lugea,Stephen J. Pandol.A Starring Role for Stellate Cells in the Pancreatic Cancer Microenvironment[J].Gastroenterology.2013(6)
  • 6Kentaro Shikata,Toshiharu Ninomiya,Yutaka Kiyohara.Diabetes mellitus and cancer risk: Review of the epidemiological evidence[J].Cancer Sci.2012(1)
  • 7Daniel Ansari,Carlos Urey,Chinmay Gundewar,Monika Posaric Bauden,Roland Andersson.Comparison of MUC4 expression in primary pancreatic cancer and paired lymph node metastases[J].Scandinavian Journal of Gastroenterology.2013(10)
  • 8Daniel Ansari,Bobby Tingstedt,Roland Andersson.Pancreatic cancer – cost for overtreatment with gemcitabine[J].Acta Oncologica.2013(6)
  • 9Ilya Gukovsky,Ning Li,Jelena Todoric,Anna Gukovskaya,Michael Karin.Inflammation, Autophagy, and Obesity: Common Features in the Pathogenesis of Pancreatitis and Pancreatic Cancer[J].Gastroenterology.2013(6)
  • 10Volker Heinemann,Michael Haas,Stefan Boeck.Systemic treatment of advanced pancreatic cancer[J].Cancer Treatment Reviews.2011(7)

引证文献10

二级引证文献21

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