The Role of Phosphatidylinositol 3-Kinase Signaling Pathways in Pancreatic Cancer

被引:12
作者
Sun, Chen [4 ]
Rosendahl, Ann H.
Andersson, Roland [1 ,2 ]
Wu, DeQuan [3 ,4 ]
Wang, Xiangdong [5 ]
机构
[1] Skane Univ Hosp Lund, Dept Surg, SE-22185 Lund, Sweden
[2] Lund Univ, Dept Surg, SE-22185 Lund, Sweden
[3] Second Affiliated Hosp, Harbin, Peoples R China
[4] Harbin Med Univ, Harbin, Peoples R China
[5] Fudan Univ, Zhongshan Hosp Ctr Lab, Shanghai 200433, Peoples R China
关键词
Pancreatic cancer; PI3K; Signaling pathway; NF-KAPPA-B; SST2 SOMATOSTATIN RECEPTOR; FATTY-ACID SYNTHASE; GROWTH-FACTOR; INDUCED APOPTOSIS; C-MYC; DUCTAL ADENOCARCINOMA; ANTITUMOR-ACTIVITY; AKT ACTIVATION; CELL LUNG;
D O I
10.1159/000327715
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Pancreatic cancer is a highly malignant cancer and the fourth leading cause of cancer-related death. It is characterized by a rapid disease progression, a highly invasive tumor phenotype, and frequently resistance to chemotherapy. Despite significant advances in diagnosis, staging, and surgical management of the disease during the past decade, prognosis of pancreatic cancer is still dismal. Methods and Results: The phosphatidylinositol 3-kinase (PI3K) signaling pathways regulate cellular growth, metabolism, survival, and motility in pancreatic cancer. Pancreatic cancer is associated with a high degree of genetic alterations that can result in aberrant activation of the PI3K signaling pathway. Elucidating the role of the PI3K signaling pathway in pancreatic cancer may thus be both meaningful and necessary. Conclusion: Improved knowledge of the PI3K signaling pathway in pancreatic cancer would furthermore be helpful in understanding mechanisms of tumor initiation and progression, and in identifying appropriate targeted anticancer treatment in pancreatic cancer. Copyright (C) 2011 S. Karger AG, Basel and IAP
引用
收藏
页码:252 / 260
页数:9
相关论文
共 97 条
  • [1] Oncogenic K-ras drives cell cycle progression and phenotypic conversion of primary pancreatic duct epithelial cells
    Agbunag, C
    Bar-Sagi, D
    [J]. CANCER RESEARCH, 2004, 64 (16) : 5659 - 5663
  • [2] Cross-talk between phosphatidylinositol 3-kinase/AKT and c-Jun NH2-terminal kinase mediates survival of isolated human islets
    Aikin, R
    Maysinger, D
    Rosenberg, L
    [J]. ENDOCRINOLOGY, 2004, 145 (10) : 4522 - 4531
  • [3] Insulin receptor substrate is a mediator of phosphoinositide 3-kinase activation in quiescent pancreatic cancer cells
    Asano, T
    Yao, YX
    Shin, S
    McCubrey, S
    Abbruzzese, JL
    Reddy, SAG
    [J]. CANCER RESEARCH, 2005, 65 (20) : 9164 - 9168
  • [4] The PI 3-kinase/Akt signaling pathway is activated due to aberrant Pten expression and targets transcription factors NF-κB and c-Myc in pancreatic cancer cells
    Asano, T
    Yao, YX
    Zhu, JJ
    Li, DH
    Abbruzzese, JL
    Reddy, SAG
    [J]. ONCOGENE, 2004, 23 (53) : 8571 - 8580
  • [5] Oncogenic PI3K deregulates transcription and translation
    Bader, AG
    Kang, SY
    Zhao, L
    Vogt, PK
    [J]. NATURE REVIEWS CANCER, 2005, 5 (12) : 921 - 929
  • [6] Gastrointestinal growth factors and hormones have divergent effects on Akt activation
    Berna, Marc J.
    Tapia, Jose A.
    Sancho, Veronica
    Thill, Michelle
    Pace, Andrea
    Hoffmann, K. Martin
    Gonzalez-Fernandez, Lauro
    Jensen, Robert T.
    [J]. CELLULAR SIGNALLING, 2009, 21 (04) : 622 - 638
  • [7] Hypoxia-reoxygenation increase invasiveness of PANC-1 cells through Rac1/MMP-2
    Binker, Marcelo G.
    Binker-Cosen, Andres A.
    Richards, Daniel
    Gaisano, Herbert Y.
    de Cosen, Rodica H.
    Cosen-Binker, Laura I.
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2010, 393 (03) : 371 - 376
  • [8] EGF promotes invasion by PANC-1 cells through Racl/ROS-dependent secretion and activation of MMP-2
    Binker, Marcelo G.
    Binker-Cosen, Andres A.
    Richards, Daniel
    Oliver, Brenda
    Cosen-Binker, Laura I.
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2009, 379 (02) : 445 - 450
  • [9] Bondar VM, 2002, MOL CANCER THER, V1, P989
  • [10] Rapamycin synergizes with the epidermal growth factor receptor inhibitor erlotinib in non-small-cell lung, pancreatic, colon, and breast tumors
    Buck, Elizabeth
    Eyzaguirre, Alexandra
    Brown, Eric
    Petti, Filippo
    McCormack, Siobhan
    Haley, John D.
    Iwata, Kenneth K.
    Gibson, Neil W.
    Griffin, Graeme
    [J]. MOLECULAR CANCER THERAPEUTICS, 2006, 5 (11) : 2676 - 2684