Evaluation of signal transduction pathways mediating the nuclear exclusion of the androgen receptor by melatonin

Cell Mol Life Sci. 2001 Dec;58(14):2129-35. doi: 10.1007/PL00000842.

Abstract

The intracellular signaling pathways mediating the nuclear exclusion of the androgen receptor (AR) by melatonin were evaluated in PC3 cells stably transfected with the AR. The melatonin-induced nuclear exclusion of the AR by melatonin (100 nM, 3 h) was blocked by LY 83583 (an inhibitor of guanylyl cyclases). 8-Bromo-cGMP (a cell-permeable cGMP analog), mimicked the effect of melatonin, as did ionomycin (a calcium ionophore) and PMA [an activator of protein kinase C (PKC)], and their effects were blocked by GF- 109203X (a selective PKC inhibitor). BAPTA (an intracellular calcium chelator) blocked the effects of melatonin and 8-bromo-cGMP but not of PMA. Inhibition or activation of the protein kinase A pathway did not affect basal or melatonin-mediated AR localization. We conclude that the melatonin-mediated rise in cGMP elicits AR nuclear exclusion via a pathway involving increased intracellular calcium and PKC activation. These results define a novel signaling pathway that regulates AR localization and androgen responses in target cells.

MeSH terms

  • Active Transport, Cell Nucleus / drug effects
  • Aminoquinolines / pharmacology
  • Antineoplastic Agents / pharmacology
  • Cell Nucleus / metabolism*
  • Chelating Agents / pharmacology
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cyclic GMP / analogs & derivatives*
  • Cyclic GMP / metabolism
  • Cyclic GMP / pharmacology
  • Dose-Response Relationship, Drug
  • Enzyme Activators / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Ionophores / pharmacology
  • Male
  • Melatonin / pharmacology*
  • Prostatic Neoplasms / metabolism*
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism*
  • Signal Transduction* / drug effects
  • Signal Transduction* / physiology
  • Transfection
  • Tumor Cells, Cultured

Substances

  • Aminoquinolines
  • Antineoplastic Agents
  • Chelating Agents
  • Enzyme Activators
  • Enzyme Inhibitors
  • Ionophores
  • Receptors, Androgen
  • 8-bromocyclic GMP
  • 6-anilino-5,8-quinolinedione
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Cyclic GMP
  • Melatonin