Choriocarcinoma cell lines JAr and JEG-3 are model systems for the study of transformed trophoblast. Both cell lines were shown to produce galectin-1, expression of which was increased in choriocarcinoma when compared to the normal trophoblast of pregnancy. In this study the effects of synthetic glucocorticoid dexametha-sone were investigated in both JAr and JEG-3 cell lines by the MTT test, cell based ELISA, and the cell adhesion and migration tests. Viable cell number/cell proliferation of JAr cells was significantly increased after treatment with 0.1 and 1 nmol/L of dexamethasone, while proliferation of JEG-3 cells was significantly increased after treatment in the whole concentration range of dexamethasone (0.1-100 nmol/L). Galectin-1 in JAr cells was modulated by dexamethasone, which mildly, but significantly decreased production at low concentrations (0.1 and 1 nmol/L). In JEG-3 cells production of galectin-1 was significantly decreased only after treatment with 100 nmol/L of dexamethasone. Cell adhesion of JEG-3 was significantly increased in the presence of lactose, an inhibitory sugar for gal-1, while dexamethasone induced decrease of JEG-3 cell migration. These findings have shown that dexamet-hasone may affect proliferation, gal-1 production and cell migration, in a cell line specific manner. These data suggest that glucocorticoid treatment in vivo might have the potential to affect cell functions in choriocarcinoma. Horiokarcinomske ćelijske linije JAr i JEG-3 su model sistemi za ispitivanje transformisanog trofoblasta. Obe ćelijske linije eksprimiraju galektin-1, čija je povećana ekspresija pokazana u horiokarcinomima u odnosu na normalni trofoblast trudnoće. U ovom radu ispitivan je efekat sintetskog glukokortikoida deksameta-zona na JAr i JEG-3 ćelijske linije, upotrebom MTT testa, ELISA testa na ćelijama i testovima adhezije i migracije. Broj živih ćelija, kao indikator proliferacije ćelija, značajno je povećan nakon tretmana 0,1 i 1 nmol/L deksametazonom, a proliferacija JEG-3 je značajno povećana u čitavom opsegu upotrebljenih koncentracija deksametazona (0,1-100 nmol/L). Galektin-1 je u JAr moduliran deksa-metazonom, koji blago, ali značajno smanjuje produkciju galektina-1 u niskim koncentracijama (0,1 i 1 nmol/L). Kod JEG-3 ćelija, produkcija galektina-1 je značajno smanjena samo nakon tretmana 100 nmol/L deksametazonom. U prisustvu laktoze kao inhibitornog šećera za ga-lektin-1 adhezija JEG-3ćelija je značajno povećana, dok deksametazon uz to smanjuje i migraciju JEG-3 ćelija. Rezultati dobijeni u ovom radu pokazuju da deksametazon utiče na proliferaciju i u manjoj meri na galektin-1 kod JAr i JEG-3 ćelija, na način specifičan za ćelijsku liniju. Dobijeni podaci ukazuju na to da bi tretman glukokortikoidima in vivo mogao imati uticaja na ćelije horiokarcinoma.