We have recently demonstrated that the alkaloid colchicine (COL) inhibits glucocorticoid receptor (GR) transcriptional activity. In addition, we described proteasome-mediated degradation of GR in COL-treated HeLa cells. While these effects were previously attributed to cell cycle arrest in G2/M phase, this explanation is not applicable for nonproliferating cells such as human hepatocytes (HH). In the current study, we compared COL-mediated microtubule disruption and cell cycle arrest with selected GR functions in HeLa cells and HH as models of proliferating and quiescent cells, respectively. Microtubule disruption led to irreversible decrease in GR binding capacity and protein level in HeLa cells. None of the parameters was restored 24 hours after COL withdrawal. In contrast, dexamethasone (DEX) binding was increased in HH at the beginning of the treatment, with following transient activation of extracellular signal-regulated kinase (ERK). The findings of these investigations emphasize the GR-signaling differences between primary and transformed cells.

• MeSH
• aktivace enzymů MeSH
• buněčný cyklus účinky léků   MeSH
• časové faktory MeSH
• dexamethason metabolismus   MeSH
• extracelulárním signálem regulované MAP kinasy metabolismus   MeSH
• fluorescenční mikroskopie MeSH
• HeLa buňky MeSH
• hepatocyty účinky léků   metabolismus   ultrastruktura   MeSH
• kolchicin farmakologie   MeSH
• lidé MeSH
• ligandy MeSH
• mikrotubuly účinky léků   ultrastruktura   MeSH
• modulátory tubulinu farmakologie   MeSH
• proliferace buněk účinky léků   MeSH
• průtoková cytometrie MeSH
• receptory glukokortikoidů metabolismus   fyziologie   MeSH
• signální transdukce účinky léků   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH