![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
A more recent version of this article appeared on October 1, 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on April 23, 2004
Revised on June 17, 2004
Accepted on July 20, 2004
Laboratory of Cell Morphogenesis and Tumor Progression, UMR 144 CNRS, Institut Curie, Section de recherche, 75248 Paris Cedex 05, France
Monitoring Editor: Carl-Henrik Heldin
FGF-1 and FGF-2 have potent biological activities implicated in malignant tumor development. Their autocrine and nonautocrine activity in tumor progression of carcinoma was investigated in the NBT-II cell system. Cells were manipulated to either produce and be autocrine for FGF-1 or FGF-2 or to only produce but not respond to these factors. The autocrine cells are highly invasive and tumorigenic and the determination of specific targets of FGF/FGFR signaling was assessed. In vitro studies showed that nonautocrine cells behave like epithelial parental cells, while autocrine cells have a mesenchymal phenotype correlated with the overexpression of uPAR, the internalization of E-cadherin and the redistribution of 
-catenin from the cell surface to the cytoplasm and nucleus. UPAR was defined as an early target, while E-cadherin and the LAR-PTP protein tyrosine phosphatase were later targets of FGF signaling, with FGFR1 activation more efficient than FGFR2 at modulating these targets. Behavior of autocrine cells was consistent with a decrease of tumor suppressive activities of both E-cadherin and LAR-PTP. These molecular analyses show that the potential of these two growth factors in tumor progression is highly dependent upon specific FGFR signaling and highlights its importance as a target for antitumor therapy.
This article has been cited by other articles:
|
|
 |
|
  R. Pai, D. Dunlap, J. Qing, I. Mohtashemi, K. Hotzel, and D. M. French Inhibition of Fibroblast Growth Factor 19 Reduces Tumor Growth by Modulating {beta}-Catenin Signaling Cancer Res., July 1, 2008; 68(13): 5086 - 5095. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Huang, Z. Hu, M. Li, Y. Cui, Y. Li, L. Guo, W. Jiang, and S. H. Lu ECRG2 inhibits cancer cell migration, invasion and metastasis through the down-regulation of uPA/plasmin activity Carcinogenesis, November 1, 2007; 28(11): 2274 - 2281. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Battersby, K.J. Sales, A.R. Williams, R.A. Anderson, S. Gardner, and H.N. Jabbour Seminal plasma and prostaglandin E2 up-regulate fibroblast growth factor 2 expression in endometrial adenocarcinoma cells via E-series prostanoid-2 receptor-mediated transactivation of the epidermal growth factor receptor and extracellular signal-regulated kinase pathway Hum. Reprod., January 1, 2007; 22(1): 36 - 44. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Stapelberg, N. Gellert, E. Swettenham, M. Tomasetti, P. K. Witting, A. Procopio, and J. Neuzil {alpha}-Tocopheryl Succinate Inhibits Malignant Mesothelioma by Disrupting the Fibroblast Growth Factor Autocrine Loop: MECHANISM AND THE ROLE OF OXIDATIVE STRESS J. Biol. Chem., July 8, 2005; 280(27): 25369 - 25376. [Abstract] [Full Text] [PDF]
|
|
