Beta-endorphin stimulates proliferation of small cell lung carcinoma cells in vitro via nonopioid binding sites

Exp Cell Res. 1995 Aug;219(2):471-6. doi: 10.1006/excr.1995.1254.

Abstract

The small cell lung carcinoma cell line U-1690 bound beta-endorphin via nonopioid binding sites also recognized by the C-terminal part of this opioid peptide Lys-Lys-Gly-Glu, but not by opiate alkaloids such as naloxone and morphine or other opioid peptides. The beta-endorphin binding did not affect the production of cAMP, but was enhanced by dexamethasone pretreatment. The beta-endorphin-stimulated proliferation of U-1690 cells was inhibited by Lys-Lys-Gly-Glu and increased by dexamethasone pretreatment. The cells also produce beta-endorphin, suggesting an autocrine mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Binding Sites
  • Carcinoma, Small Cell / metabolism*
  • Carcinoma, Small Cell / pathology*
  • Cell Division / drug effects
  • Cyclic AMP / biosynthesis
  • Humans
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / pathology*
  • Molecular Sequence Data
  • Narcotics / metabolism
  • beta-Endorphin / pharmacology*

Substances

  • Narcotics
  • beta-Endorphin
  • Cyclic AMP