期刊文献+

LY294002 Enhances Inhibitory Effect of Gemcitabine on Proliferation of Human Pancreatic Carcinoma PANC-1 Cells

LY294002 Enhances Inhibitory Effect of Gemcitabine on Proliferation of Human Pancreatic Carcinoma PANC-1 Cells
下载PDF
导出
摘要 Phosphatidylinositide 3-kinase (PI3K)/protein kinase B (PKB, Akt) pathway plays a major role in proliferation and survival of many types of cells. The inhibitory effect of LY294002, widely ap- plied as an inhibitor of PI3K, in combination with gemcitabine on proliferation of PANC-1 ceils was investigated. The expression of PI3K, phosphorylated AM (p-Akt) and multidrng-resistance like protein (MRP) in normal pancreas tissues, chronic pancreatitis tissues and pancreatic carcinoma tissues was de- tected. The effects of LY294002 combined with gemcitabine on proliferation of PANC-1 cells and pro- tein levels of p-Akt and MRP were detected. The results showed that the positive expression rate of PI3K, p-Akt and MRP in pancreatic carcinoma tissues was significantly higher than that in normal pan- creas tissues and chronic pancreatitis tissues (P〈0.01 and P〈0.05 respectively). LY294002 could effec- tively enhance the inhibitory effect of gemcitabine on proliferation of PANC-1 cells. Furthermore, Western blotting revealed that LY294002 combined with gemcitabine reduced the protein levels of p-Akt and MRP, which contributed to the inhibition of proliferation. It is concluded that LY294002 in combination with gemcitabine may represent an alternative therapy for pancreatic carcinoma. Phosphatidylinositide 3-kinase (PI3K)/protein kinase B (PKB, Akt) pathway plays a major role in proliferation and survival of many types of cells. The inhibitory effect of LY294002, widely ap- plied as an inhibitor of PI3K, in combination with gemcitabine on proliferation of PANC-1 ceils was investigated. The expression of PI3K, phosphorylated AM (p-Akt) and multidrng-resistance like protein (MRP) in normal pancreas tissues, chronic pancreatitis tissues and pancreatic carcinoma tissues was de- tected. The effects of LY294002 combined with gemcitabine on proliferation of PANC-1 cells and pro- tein levels of p-Akt and MRP were detected. The results showed that the positive expression rate of PI3K, p-Akt and MRP in pancreatic carcinoma tissues was significantly higher than that in normal pan- creas tissues and chronic pancreatitis tissues (P〈0.01 and P〈0.05 respectively). LY294002 could effec- tively enhance the inhibitory effect of gemcitabine on proliferation of PANC-1 cells. Furthermore, Western blotting revealed that LY294002 combined with gemcitabine reduced the protein levels of p-Akt and MRP, which contributed to the inhibition of proliferation. It is concluded that LY294002 in combination with gemcitabine may represent an alternative therapy for pancreatic carcinoma.
出处 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2013年第1期57-62,共6页 华中科技大学学报(医学英德文版)
关键词 pancreatic carcinoma phosphatidylinositide 3-kinase phosphorylated protein kinase B multidrug-resistance like protein LY294002 pancreatic carcinoma phosphatidylinositide 3-kinase phosphorylated protein kinase B multidrug-resistance like protein LY294002
  • 相关文献

参考文献1

二级参考文献10

  • 1Kandel ES,Skeen J,Majewski N,et al.Activation of Akt/protein kinase B overcomes a G(2)/m cell cycle checkpoint induced by DNA damage[].Molecular and Cellular Probes.2002
  • 2Clark AS,West K,Streicher S, et al.Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells[].Molecular Cancer.2002
  • 3Fairbairn DW,Olive PL,O’Neill KL.Comet assay, a comprehensive review[].Mutation Research.1995
  • 4Singh N P,Stephens R E.Microgel electrophoresis: sensitivity, mechanisms, and DNA electrostretching[].Mutation Research.1997
  • 5Jin ZH,Kurosu T,Yamaguchi M,et al.Hematopoietic cytokines enhance Chk1-dependent G2/M checkpoint activation by etoposide through the Akt/GSK3pathway to inhibit apoptosis[].Oncegene.2005
  • 6CHENGJ Q,LI NDSLEY C W,CHENG GZ,et al.The Akt/PKB pathway:molecular target for cancer drug discovery[].Oncegene.2005
  • 7Opel D,Westhoff MA,Bender A,Braun V,Debatin KM,Fulda S.Phosphatidylinositol 3-kinase inhibition broadly sensitizes glioblastoma cells to death receptor- and drug-induced apoptosis[].Cancer Research.2008
  • 8Okumura,E,Fukuhara,T,Yoshida,H,Hanada Si,S,Kozutsumi,R,Mori,M,Tachibana,K,Kishimoto,T.Akt inhibits Myt1 in the signalling pathway that leads to meiotic G2/M-phase transition[].Nature Cell Biology.2002
  • 9Tan J,Hallahan DE.Growth factor-independent activation of protein kinase B contributes to the inherent resistance of vascular endothelium to radiation-induced apoptotic response[].Cancer Research.2003
  • 10Riesterer O,Tenzer A,Zingg D,et al.Novel radiosensitizers for locally advanced epithelial tumors: inhibition of the PI3K/AKT survival pathway in tumor cells and in tumor-associated endothelial cells as a novel treatment strategy[].International Journal of Radiation Oncology Biology Physics.2004

共引文献3

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