Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Tumor-Suppressor Function of Muscarinic Acetylcholine Receptors is Associated with Activation of Receptor-Operated Calcium Influx

Christian C. Felder, Linda MacArthur, Alice L. Ma, Fabian Gusovsky and Elise C. Kohn
Proceedings of the National Academy of Sciences of the United States of America
Vol. 90, No. 5 (Mar. 1, 1993), pp. 1706-1710
Stable URL: http://www.jstor.org/stable/2361386
Page Count: 5
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Tumor-Suppressor Function of Muscarinic Acetylcholine Receptors is Associated with Activation of Receptor-Operated Calcium Influx
Preview not available

Abstract

Several members of the family of guanine nucleotide-binding protein (G protein)-coupled receptors have recently been shown to induce agonist-dependent foci development in NIH 3T3 cells and tumors in nude mice. We selected the five subtypes of the muscarinic acetylcholine receptor family to investigate their role in tumor suppression. When transfected and expressed in CHO-K1 Chinese hamster ovary cells, m1, m3, and m5 muscarinic acetylcholine receptor activation resulted in a morphology change. Receptor activation did not slow or inhibit monolayer growth of CHOm5 cells in culture but markedly inhibited density-independent growth in soft agar and suppressed tumor formation in nude mice. Receptor-mediated tumor suppression was found to be agonist-dependent and reversible and was blocked with a muscarinic receptor antagonist. Of the five signaling pathways associated with the m1, m3, and m5 receptors, only receptor-operated, and inositol trisphosphate-independent, calcium influx was found to correlate with inhibition of tumorigenicity. These data suggest a pivotal role for inositol trisphosphate-independent receptor-regulated calcium homeostasis in CHO-K1 tumor suppression.

Page Thumbnails

  • Thumbnail: Page 
1706
    1706
  • Thumbnail: Page 
1707
    1707
  • Thumbnail: Page 
1708
    1708
  • Thumbnail: Page 
1709
    1709
  • Thumbnail: Page 
1710
    1710