%0 Journal Article %T Phosphorylation of JAK2 by serotonin 5-HT (2A) receptor activates both STAT3 and ERK1/2 pathways and increases growth of JEG-3 human placental choriocarcinoma cell. %+ Institut Armand Frappier (INRS-IAF) %A Oufkir, T. %A Vaillancourt, Cathy %Z This work is financially supported by a Natural Sciences and Engineering Research Council of Canada e discovery grant (NSERC # 262011-2009). %< avec comité de lecture %@ 0143-4004 %J Placenta %I Elsevier %V 32 %N 12 %P 1033-40 %8 2011-12 %D 2011 %R 10.1016/j.placenta.2011.09.005 %M 21993263 %Z Life Sciences [q-bio]/ToxicologyJournal articles %X Serotonin 5-HT(2A) receptor activation improves viability, increases DNA synthesis and activates JAK2-STAT3 and MEK1/2-ERK1/2 signalling pathways in JEG-3 human trophoblast choriocarcinoma cells. The goal of this study was to characterize the signal transduction cascade involved in 5-HT(2A) receptor-induced growth of JEG-3 cells. Selective 5-HT(2A) receptor agonist, DOI, induced JEG-3 cell growth was inhibited by the inhibitor of JAK2 (AG490), MEK1/2 (U0126), phospholipase C-β (PLC-β; U73122) and protein kinase C-β (PKC-β; Gö6976)), whereas the selective phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) had no effect. Specific inhibitors of PLC-β, PKC-β and Ras (farnesylthiosalicylic acid) inhibit activation of ERK1/2, whereas the PKC-ζ inhibitor GF109203X had no effect. Interestingly, inhibition of JAK2 prevented DOI-induced phosphorylation of ERK1/2 whereas inhibition of ERK1/2 pathway had no effect on DOI-induced activation of STAT3. Taken together, our results demonstrate that both the JAK2-STAT3 and PLC-β-PKC-β-Ras-ERK1/2 signalling pathways are involved in the stimulation of JEG-3 cell growth mediated by DOI. Moreover, this study shows that activation of JAK2 by the 5-HT(2A) receptor is essential to activate both STAT3 and ERK1/2 signalling pathways as well as to increase JEG-3 choriocarcinoma cell growth and survival. %G English %L pasteur-00723284 %U https://riip.hal.science/pasteur-00723284 %~ RIIP %~ INRS-IAF