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Comparative effects of microtubules disruption on glucocorticoid receptor functions in proliferating and quiescent

Radim Vrzal1, Sabine Gerbal-Chaloin, Patrick Maurel

  • 1Department of Cell Biology and Genetics, Faculty of Science, Palacký University Olomouc, Slechtitelů 11, Olomouc, Czech Republic. radim.vrzal@email.cz

International Journal of Toxicology
|May 8, 2010
PubMed

Insights

Colchicine (COL) disrupts microtubules, inhibiting glucocorticoid receptor (GR) activity and protein levels in proliferating HeLa cells. However, quiescent human hepatocytes show increased GR binding and transient ERK activation, highlighting cell-specific GR signaling differences.

Area of Science:

  • Cell Biology
  • Molecular Pharmacology
  • Biochemistry

Background:

  • Alkaloid colchicine (COL) is known to inhibit glucocorticoid receptor (GR) transcriptional activity and induce proteasome-mediated GR degradation.
  • These effects were previously attributed to cell cycle arrest in G2/M phase, a mechanism not applicable to nonproliferating cells.

Purpose of the Study:

  • To compare colchicine-mediated microtubule disruption and cell cycle arrest with selected GR functions in proliferating HeLa cells and quiescent human hepatocytes.
  • To investigate cell-specific differences in GR signaling pathways.

Main Methods:

  • Comparison of microtubule disruption, cell cycle arrest, and GR functions (binding capacity, protein level, dexamethasone binding) in HeLa cells and human hepatocytes.
  • Assessment of extracellular signal-regulated kinase (ERK) activation in response to dexamethasone treatment.

Main Results:

  • Microtubule disruption by colchicine caused an irreversible decrease in GR binding capacity and protein level in HeLa cells, with no recovery after drug withdrawal.
  • In contrast, human hepatocytes exhibited increased dexamethasone (DEX) binding initially, followed by transient extracellular signal-regulated kinase (ERK) activation.
  • These findings indicate distinct GR signaling responses between primary and transformed cells.

Conclusions:

  • Colchicine's effects on GR signaling differ significantly between proliferating (HeLa) and quiescent (human hepatocytes) cells.
  • Microtubule disruption impacts GR in HeLa cells, while human hepatocytes display unique responses involving DEX binding and ERK activation.
  • The study underscores fundamental differences in GR signaling between primary and transformed cell types.

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