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

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.

• Authors: M F Melzig, I Nylander, M Vlaskovska, L Terenius
• Journal: Experimental cell research (Exp Cell Res) Vol. 219 Issue 2 Pg. 471-6 (Aug 1995) ISSN: 0014-4827 [Print] United States
• PMID: 7641799 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Narcotics
• beta-Endorphin
• Cyclic AMP

Topics

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