Activation of muscarinic acetylcholine receptors inhibits cell cycle progression of small cell lung carcinoma. Cell Regul 1991 May;2(5):373-81
Date
05/01/1991Pubmed ID
1654127Pubmed Central ID
PMC361805DOI
10.1091/mbc.2.5.373Scopus ID
2-s2.0-0026164317 (requires institutional sign-in at Scopus site) 44 CitationsAbstract
We previously reported that activation of muscarinic acetylcholine receptors (mAChR) of M3 subtype causes hydrolysis of phosphoinositides and inhibits voltage-gated Ca2+ channel activity in small cell lung carcinoma (SCLC) cells. We now report that mAChR activation causes exponentially growing SCLC cells to arrest in S and G2/M phases of the cell cycle, concomitant with a decrease in DNA synthesis. Cell cycle progression and DNA synthesis resume when mAChR are down-regulated. In serum-starved SCLC cells, mAChR activation inhibits DNA synthesis induced by serum, bombesin, insulin, or insulin-like growth factor-I. The finding that DNA synthesis is inhibited even when mAChR are activated after exposure of cells to growth factors indicates that decreased signal transduction by growth factor receptors is not the mechanism of mAChR-mediated growth inhibition. Our data suggest that mAChR activation disrupts a common event that is induced by different growth factors and is fundamental for cell cycle progression.
Author List
Williams CL, Lennon VAAuthor
Carol L. Williams PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
BombesinCalcium
Carbachol
Carcinoma, Small Cell
Cell Cycle
Cell Division
Culture Media
DNA
Down-Regulation
Humans
Insulin
Insulin-Like Growth Factor I
Receptors, Cholinergic
Signal Transduction
Tumor Cells, Cultured
