scholarly journals The effect of tyrphostins AG494 and AG1478 on the autocrine growth regulation of A549 and DU145 cells

2012 ◽  
Vol 50 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Agnieszka Bojko ◽  
Kinga Reichert ◽  
Anna Adamczyk ◽  
Joanna Ligęza ◽  
Janusz Ligęza ◽  
...  
Keyword(s):  
Growth Regulation ◽  
Autocrine Growth ◽  
Autocrine Growth Regulation ◽  
Du145 Cells

Autocrine Growth Regulation in Neuroectodermal Tumors as Detected with Oligodeoxynucleotide Antisense Molecules

Neurosurgery ◽  
1993 ◽  
Vol 33 (4) ◽  
pp. 679-684 ◽  
Author(s):  
Christian Behl ◽  
Juergen Winkler ◽  
Ulrich Bogdahn ◽  
Juergen Meixensberger ◽  
Karl-Herrman Schligensiepen ◽  
...  
Keyword(s):  
Growth Regulation ◽  
Autocrine Growth ◽  
Neuroectodermal Tumors ◽  
Autocrine Growth Regulation

Autocrine Growth Regulation in Fetal and Adult Human Fibroblasts

1997 ◽  
Vol 237 (2) ◽  
pp. 348-353 ◽  
Author(s):  
Harris Pratsinis ◽  
Dimitris Kletsas ◽  
Dimitri Stathakos
Keyword(s):  
Growth Regulation ◽  
Human Fibroblasts ◽  
Autocrine Growth ◽  
Adult Human ◽  
Autocrine Growth Regulation

Autocrine Growth Regulation in Neuroectodermal Tumors as Detected with Oligodeoxynucleotide Antisense Molecules

Neurosurgery ◽  
1993 ◽  
Vol 33 (4) ◽  
pp. 679-684 ◽  
Author(s):  
Christian Behl ◽  
Juergen Winkler ◽  
Ulrich Bogdahn ◽  
Juergen Meixensberger ◽  
Karl-Herrman Schligensiepen ◽  
...  
Keyword(s):  
Growth Regulation ◽  
Autocrine Growth ◽  
Neuroectodermal Tumors ◽  
Autocrine Growth Regulation

scholarly journals Growth factor/growth factor receptor loops in autocrine growth regulation of human prostate cancer DU145 cells.

2011 ◽  
Vol 58 (3) ◽  
Author(s):  
Janusz Ligęza ◽  
Joanna Ligęza ◽  
Andrzej Klein
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Growth Regulation ◽  
Growth Factor Receptor ◽  
Human Prostate ◽  
Main Step ◽  
Autocrine Growth ◽  
Du145 Cells

Autocrine growth factors produced by epithelial cells mediate the development and proliferation of neoplastic human prostate tissue. Various approaches have been used to down-regulate neoplastic growth of prostate cancer using natural flavonoids, soluble receptors, pseudo-ligands, monoclonal antibodies and tyrosine kinase inhibitors (tyrphostins). Selected growth factor/growth factor receptor loops (mainly TGFα/EGFR and IGFs/IGFIR) have been proposed as regulators of prostate cancer cell growth. We have previously determined that blockade of IGFIR or VEGF2R signaling pathways by tyrphostin AG1024 and SU1498 inhibits autocrine growth and viability of DU145 cells in vitro. Recently, we compared the activity of AG1024 and SU1498 with the inhibiting effect of tyrphostin A23 (a selective inhibitor of EGFR). The results described in this paper confirm that DU145 cells do not produce IGFI or EGF. In contrast, DU145 cells produce a great amount of VEGF, much more than TGFα (about 60-fold), and VEGF may be the real autocrine growth factor of the investigated cells. The results indicate that the growth of DU145 may be regulated by at least three autocrine loops: TGFα/EGFR, IGFII/IGFIR and VEGF/VEGFR2. Neither AG1024 nor SU1498 affected the production of TGFα substantially, which excludes the possibility that IGFRs or VEGFR2 inhibitors arrest the growth of these cells by inhibition of synthesis and/or secretion of TGFα. The obtained data indicate that all tree investigated tyrphostins (AG1024, SU1498 and A23) inhibit signal transmission by Akt (PKB), ERK(1/2), Src and STAT in a similar manner. A comparison of the effects of the investigated tyrphostins indicates that TGFα, IGFII and VEGF stimulate cell growth by affecting the same signaling pathway. The hypothesis was confirmed by the effect of the investigated tyrphostins on activation of EGFR. All these inhibitors decreased phosphorylation of EGFR to the same extent, and after the same time of incubation with cell culture. These results strongly suggest that stimulation of EGFR kinase is the main step in the initiation of mitogen signaling in DU145 cells, regardless of the type of ligand (TGFα, IGFs or VEGF) and their specific receptors.

Sign in / Sign up

Export Citation Format

Share Document