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Leukemia inhibitory factor triggers activation of signal transducer and activator of transcription 3, proliferation, invasiveness, and altered protease expression in choriocarcinoma cells

Fitzgerald, Justine S.; Tsareva, Svetlana A.; Poehlmann, Tobias G.; Berod, Luciana; Meissner, Anja LU ; Corvinus, Florian M.; Wiederanders, Bernd; Pfitzner, Edith; Markert, Udo R. and Friedrich, Karlheinz (2005) In International Journal of Biochemistry and Cell Biology 37(11). p.2284-2296
Abstract

Extravillous trophoblast cells resemble cancer cells with regard to their intrinsic invasiveness. They invade decidual tissue, but, unlike tumor cells, shut down their invasive properties, when they become inappropriate. Stimuli involved in the modulation of invasion, as well as their underlying signaling mechanisms require further clarification. We were especially interested in discovering signals capable of stimulating invasion in otherwise low-invasive cells involved in reproduction. Using the choriocarcinoma cell line Jeg-3 as a model, we have addressed the potential role of cytokine/growth factor-driven activation of signal transducer and activator of transcription 3 (STAT3) in this process. Jeg-3 cells were treated with various... (More)

Extravillous trophoblast cells resemble cancer cells with regard to their intrinsic invasiveness. They invade decidual tissue, but, unlike tumor cells, shut down their invasive properties, when they become inappropriate. Stimuli involved in the modulation of invasion, as well as their underlying signaling mechanisms require further clarification. We were especially interested in discovering signals capable of stimulating invasion in otherwise low-invasive cells involved in reproduction. Using the choriocarcinoma cell line Jeg-3 as a model, we have addressed the potential role of cytokine/growth factor-driven activation of signal transducer and activator of transcription 3 (STAT3) in this process. Jeg-3 cells were treated with various factors known to induce trophoblast proliferation, differentiation, migration, or invasiveness (insulin-like-growth-factor-II (IGF-II), hepatocyte growth factor (HGF), interleukin-6 (IL-6), and leukemia inhibitory factor (LIF)). Only LIF elicited strong tyrosine phosphorylation and specific DNA-binding activity of STAT3. It induced a significant acceleration of cell proliferation and promoted the capability of Jeg-3 cells to invade into an artificial extracellular matrix. Moreover, LIF influenced the expression pattern of proteases and protease inhibitors with potential relevance for invasiveness (downregulation of mRNA for tissue inhibitor of metalloproteinase 1 (TIMP-1) and upregulation of mRNA for caspase-4). In conjunction with earlier work, in which we found that STAT3 DNA-binding activity was increased in invasive cells (choriocarcinoma, first trimester trophoblasts) and absent in non-invasive cells (term trophoblasts), these findings suggest a connection between LIF-driven STAT3 activity and invasiveness of choriocarcinoma and trophoblast cells.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Choriocarcinoma, Invasion, LIF, STAT3, Trophoblast
in
International Journal of Biochemistry and Cell Biology
volume
37
issue
11
pages
13 pages
publisher
Elsevier
external identifiers
  • scopus:23944433875
ISSN
1357-2725
DOI
10.1016/j.biocel.2005.02.025
language
English
LU publication?
no
id
9a2e49d5-6bb3-4df7-95a4-e7a6cb30f5cb
date added to LUP
2017-05-23 22:27:14
date last changed
2017-09-17 09:47:07
@article{9a2e49d5-6bb3-4df7-95a4-e7a6cb30f5cb,
  abstract     = {<p>Extravillous trophoblast cells resemble cancer cells with regard to their intrinsic invasiveness. They invade decidual tissue, but, unlike tumor cells, shut down their invasive properties, when they become inappropriate. Stimuli involved in the modulation of invasion, as well as their underlying signaling mechanisms require further clarification. We were especially interested in discovering signals capable of stimulating invasion in otherwise low-invasive cells involved in reproduction. Using the choriocarcinoma cell line Jeg-3 as a model, we have addressed the potential role of cytokine/growth factor-driven activation of signal transducer and activator of transcription 3 (STAT3) in this process. Jeg-3 cells were treated with various factors known to induce trophoblast proliferation, differentiation, migration, or invasiveness (insulin-like-growth-factor-II (IGF-II), hepatocyte growth factor (HGF), interleukin-6 (IL-6), and leukemia inhibitory factor (LIF)). Only LIF elicited strong tyrosine phosphorylation and specific DNA-binding activity of STAT3. It induced a significant acceleration of cell proliferation and promoted the capability of Jeg-3 cells to invade into an artificial extracellular matrix. Moreover, LIF influenced the expression pattern of proteases and protease inhibitors with potential relevance for invasiveness (downregulation of mRNA for tissue inhibitor of metalloproteinase 1 (TIMP-1) and upregulation of mRNA for caspase-4). In conjunction with earlier work, in which we found that STAT3 DNA-binding activity was increased in invasive cells (choriocarcinoma, first trimester trophoblasts) and absent in non-invasive cells (term trophoblasts), these findings suggest a connection between LIF-driven STAT3 activity and invasiveness of choriocarcinoma and trophoblast cells.</p>},
  author       = {Fitzgerald, Justine S. and Tsareva, Svetlana A. and Poehlmann, Tobias G. and Berod, Luciana and Meissner, Anja and Corvinus, Florian M. and Wiederanders, Bernd and Pfitzner, Edith and Markert, Udo R. and Friedrich, Karlheinz},
  issn         = {1357-2725},
  keyword      = {Choriocarcinoma,Invasion,LIF,STAT3,Trophoblast},
  language     = {eng},
  number       = {11},
  pages        = {2284--2296},
  publisher    = {Elsevier},
  series       = {International Journal of Biochemistry and Cell Biology},
  title        = {Leukemia inhibitory factor triggers activation of signal transducer and activator of transcription 3, proliferation, invasiveness, and altered protease expression in choriocarcinoma cells},
  url          = {http://dx.doi.org/10.1016/j.biocel.2005.02.025},
  volume       = {37},
  year         = {2005},
}