STAT3 and ERK1/2 Cross-talk in Leukaemia Inhibitory Factor Mediated Trophoblastic JEG-3 Cell Invasion and Expression of Mucin 1 and Fos
Article first published online: 10 APR 2014
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 72, Issue 1, pages 65–74, July 2014
How to Cite
STAT3 and ERK1/2 cross-talk in leukaemia inhibitory factor mediated trophoblastic JEG-3 cell invasion and expression of mucin1 and Fos. Am J Reprod Immunol 2014; 72: 65–74, .
- Issue published online: 11 JUN 2014
- Article first published online: 10 APR 2014
- Manuscript Accepted: 9 MAR 2014
- Manuscript Received: 14 JAN 2014
- National Institute of Immunology, New Delhi
- Indian Council of Medical Research, Government of India
- Leukaemia inhibitory factor;
- trophoblast invasion
The aim of this study was to investigate the relative importance of STAT3 and ERK1/2 activation in leukaemia inhibitory factor (LIF)-mediated invasion of JEG-3 cells.
Method of Study
Matrigel matrix-based invasion assay; Western blot; cDNA microarray; quantitative RT-PCR; gene silencing by siRNA.
Leukaemia inhibitory factor treatment led to the activation of STAT3 and ERK1/2 signaling pathways which was followed by changes in the expression of several invasion-associated molecules such as mucin1 (MUC1), Fos, Jun, etc. Abrogation of either STAT3 or ERK1/2 signaling reduced (P < 0.05) the LIF-mediated invasion of JEG-3 cells. It was associated with a significant reduction in the expression of both MUC1 and Fos, suggesting a common denominator in LIF-STAT3-ERK1/2 signaling. To this effect, we observed a decrease in LIF-mediated p-STAT3 (Ser727) upon blocking STAT3 or ERK1/2 signaling.
ERK1/2 as well as JAK-STAT-mediated STAT3 (Ser727) phosphorylation play an important role in LIF-mediated JEG-3 trophoblastic cell invasion and gene expression.