title: Eph-ephrin A system regulates human choriocarcinoma-derived JEG-3 cell invasion.
abstract: OBJECTIVE
  The Eph-ephrin system is a unique system that can induce multiple cellular responses such as cell migration, regulation of angiogenesis, and axonal guidance. Previously, the Eph-ephrin system was reported to regulate human extravillous trophoblast invasion. In this study, we examined the possible involvement of the Eph-ephrin system in the invasion of malignant gestational trophoblastic diseases using a human choriocarcinoma-derived cell line, JEG-3.
  
  
  METHODS
  The mRNA expression of class A Ephs and ephrins on JEG-3 cells was examined by reverse transcription-polymerase chain reaction. The effects of recombinant human Eph A1 (r-Eph A1) and r-ephrin A4 on the proliferation and invasion of JEG-3 cells were investigated by cell proliferation and Matrigel invasion assays. The alterations of integrin expression on JEG-3 cells in the presence of r-Eph A1 and r-ephrin A4 were investigated by flow cytometry. The induction of phosphorylation of focal adhesion kinase in JEG-3 cells by r-ephrin A4 was examined by Western blot analysis.
  
  
  RESULTS
  By reverse transcription-polymerase chain reaction, mRNAs of Eph A1, A2, and A4 and ephrin A1, A4, and A5 were detected on JEG-3 cells. In Matrigel invasion assay, both r-Eph A1 and r-ephrin A4 promoted the invasion of JEG-3 cells without affecting cell proliferation. During 24-hour culture with r-Eph A1 and r-ephrin A4, the increase in integrin α 5 expression on JEG-3 cells was observed by flow cytometry. Western blotting analysis showed that r-ephrin A4 induced dephosphorylation of focal adhesion kinase in JEG-3 cells.
  
  
  CONCLUSIONS
  These findings suggest that Eph-ephrin interaction plays some role in the regulation of choriocarcinoma invasion in cooperation with integrins.
authors: Department of Gynecology and Obstetrics, Faculty of Medicine, Kyoto University, Kyoto, Japan. fuji@kuhp.kyoto-u.ac.jp
authors: Hiroshi
authors: H
authors: Fujiwara
authors: Yoshihiro
authors: Y
authors: Nishioka
authors: Hisanori
authors: H
authors: Matsumoto
authors: Koh
authors: K
authors: Suginami
authors: Akihito
authors: A
authors: Horie
authors: Hirohiko
authors: H
authors: Tani
authors: Noriomi
authors: N
authors: Matsumura
authors: Tsukasa
authors: T
authors: Baba
authors: Yukiyasu
authors: Y
authors: Sato
authors: Yoshihiko
authors: Y
authors: Araki
authors: Ikuo
authors: I
authors: Konishi
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D002822:Choriocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D003094:Collagen / Q000378:metabolism; D004338:Drug Combinations; D036342:Ephrins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016023:Integrins / Q000235:genetics / Q000378:metabolism*; D007797:Laminin / Q000378:metabolism; D011247:Pregnancy; D011509:Proteoglycans / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D036081:Receptors, Eph Family / Q000235:genetics / Q000378:metabolism*; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014407:Tumor Cells, Cultured; D014594:Uterine Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
chemical_list: D004338:Drug Combinations; D036342:Ephrins; D016023:Integrins; D007797:Laminin; D011509:Proteoglycans; D012333:RNA, Messenger; D011994:Recombinant Proteins; C059485:matrigel; D003094:Collagen; D036081:Receptors, Eph Family