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The regulation of STAT3 phosphorylation at its ser727 binding site, possible crosstalk with intracellular MAPK signaling, and their functional implications are the object of the present investigation. JEG\u20103 choriocarcinoma cells were cultured in presence\/absence of LIF and the specific ERK1\/2 inhibitor (U0126). Phosphorylation of signaling molecules (p\u2010STAT3 (ser727 and tyr705) and p\u2010ERK1\/2 (thr 202\/tyr 204)) was assessed per Western blot. Immunocytochemistry confirmed results, but also pinpointed the location of phosphorylated signaling molecules. STAT3 DNA\u2010binding capacity was studied with a colorimetric ELISA\u2010based assay. Cell viability and invasion capability were assessed by MTS and Matrigel assays. Our results demonstrate that LIF\u2010induced phosphorylation of STAT3 (tyr705 and ser727) is significantly increased after blocking ERK1\/2. STAT3 DNA\u2010binding capacity and cell invasiveness are enhanced after LIF stimulation and ERK1\/2 blockage. In contrast, proliferation is enhanced by LIF but reduced after ERK1\/2 inhibition. The findings herein show that blocking ERK1\/2 increases LIF\u2010induced STAT3 phosphorylation and STAT3 DNA\u2010binding capacity by an intranuclear crosstalk, which leads to enhanced invasiveness and reduced proliferation.<\/jats:p>","DOI":"10.1155\/2013\/259845","type":"journal-article","created":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T00:23:39Z","timestamp":1383179019000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Intranuclear Crosstalk between Extracellular Regulated Kinase1\/2 and Signal Transducer and Activator of Transcription 3 Regulates JEG\u20103 Choriocarcinoma Cell Invasion and Proliferation"],"prefix":"10.1155","volume":"2013","author":[{"given":"Diana 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