Regulation of E-cadherin-mediated adhesion by muscarinic acetylcholine receptors in small cell lung carcinoma. J Cell Biol 1993 May;121(3):643-54
Date
05/01/1993Pubmed ID
8387530Pubmed Central ID
PMC2119556DOI
10.1083/jcb.121.3.643Scopus ID
2-s2.0-0027289308 (requires institutional sign-in at Scopus site) 96 CitationsAbstract
We present the first evidence that adhesion mediated by a member of the cadherin gene family can be regulated by a G protein-coupled receptor. We show that activating the M3 muscarinic acetylcholine receptor (mAChR) rapidly induces E-cadherin-mediated adhesion in a small cell lung carcinoma (SCLC) cell line. This response is inhibited by E-cadherin antibodies, and does not occur in another SCLC cell line which expresses functional mAChR but reduced levels of E-cadherin. Protein kinase C may be involved, since phorbol 12-myristate 13-acetate also induces E-cadherin-mediated aggregation. Immunofluorescence analyses indicate that mAChR activation does not grossly alter E-cadherin surface expression or localization at areas of cell-cell contact, suggesting mAChR activation may increase E-cadherin binding activity. Our findings suggest that G protein-coupled receptors may regulate processes involving cadherin-mediated adhesion, such as embryonic development, neurogenesis, and cancer metastasis.
Author List
Williams CL, Hayes VY, Hummel AM, Tarara JE, Halsey TJAuthor
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
CadherinsCarcinoma, Small Cell
Cell Adhesion
Cell Aggregation
GTP-Binding Proteins
Humans
Lung Neoplasms
Neoplasm Metastasis
Phorbol Esters
Protein Kinase C
Receptors, Muscarinic
Tumor Cells, Cultured
