Open AccessGangliosides as bimodal regulators of cell growth.
Author(s) -
Sarah Spiegel,
Peter H. Fishman
Publication year - 1987
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.84.1.141
Subject(s) - cholera toxin , 3t3 cells , cell growth , biology , ganglioside , microbiology and biotechnology , protein subunit , g alpha subunit , growth factor , epidermal growth factor , cell , biochemistry , cell culture , transfection , receptor , endocrinology , genetics , gene
The B subunit of cholera toxin, which binds specifically to several molecules of ganglioside galactosyl-(beta 1----3)-N-acetylgalactosyminyl(beta 1----4)-[N- acetylneuraminyl(alpha 2----3)]-galactosyl(beta 1----4)glucosyl(beta 1----1) ceramide (GM1) on the cell surface, stimulated DNA synthesis and cell division in quiescent, nontransformed mouse 3T3 cells in a dose-dependent manner. In addition, the B subunit potentiated the response of the 3T3 cells to other mitogens, such as epidermal growth factor, platelet-derived growth factor, and insulin. This synergistic effect indicates that the B subunit does not act identically to any of these growth factors but probably modulates a common effector system crucial for cell proliferation. In distinct contrast, the B subunit inhibited the growth of ras-transformed 3T3 cells as well as rapidly dividing normal 3T3 cells. Thus, the same cells, depending on their state of growth, exhibited a bimodal response to the B subunit. We conclude that endogenous gangliosides may be bimodal regulators of positive and negative signals for cell growth.