Choriocarcinoma cell line Response to Dexamethasone

Abstract

Kratak sadr`aj: Horiokarcinomske }elijske linije JAr i JEG-3 su model sistemi za ispitivanje transformisanog trofo blasta. Obe }elijske linije eksprimiraju galektin-1, ~ija je pove}ana ekspresija pokazana u horiokarcinomima u odno su na normalni trofoblast trudno}e. U ovom radu ispitivan je efekat sintetskog glukokortikoida deksametazona na JAr i JEG-3 }elijske linije, upotrebom MTT testa, ELISA testa na }elijama i testovima adhezije i migracije. Broj `ivih }elija, kao indikator proliferacije }elija, zna ~ajno je pove}an nakon tretmana 0,1 i 1 nmol/L deksameta zonom, a proliferacija JEG-3 je zna~ajno pove}ana u ~itavom opsegu upotrebljenih koncentracija deksameta zo na (0,1-100 nmol/L). Galektin-1 je u JAr moduliran deksametazonom, koji blago, ali zna~ajno smanjuje pro duk ciju galektina-1 u niskim koncentracijama (0,1 i 1 nmol/L). Kod JEG-3 }elija, produkcija galektina-1 je zna~ajno smanjena samo nakon tretmana 100 nmol/L deksameta zonom. U prisustvu laktoze kao inhibitornog {e}era za galektin-1 adhezija JEG-3 }elija je zna~ajno pove}ana, dok deksa metazon uz to smanjuje i migraciju JEG-3 }elija. Rezultati dobijeni u ovom radu po kazuju da deksametazon uti~e na proliferaciju i u manjoj meri na galektin-1 kod JAr i JEG-3 }elija, na na~in spe ci fi~an za }elijsku liniju. Dobijeni podaci ukazuju na to da bi tret man glukokortikoidima in vivo mogao imati uticaja na }elije horiokarcinoma. Summary: 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 dexamethasone were inves ti gated 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 signi ficantly increased after treatment with 0.1 and 1 nmol/L of dexamethasone, while proliferation of JEG-3 cells was signi ficantly 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 pro duction of galectin-1 was significantly decreased only after treat ment with 100 nmol/L of dexamethasone. Cell adhe sion of JEG-3 was significantly increased in the presence of lacto se, an inhibitory sugar for gal-1, while dexamethasone indu ced decrease of JEG-3 cell migration. These findings have shown that dexamethasone 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 cho riocarcinoma.