Transformation of BALB/3T3 cells with EJ/T24/H-ras oncogene inhibits adenylate cyclase response to beta-adrenergic agonist while increases muscarinic receptor dependent hydrolysis of inositol lipids.
Balb/3T3 murine fibroblasts transformed by transfection with the EJ/T24 human bladder carcinoma oncogene were assayed in terms of adenylate cyclase response and hydrolysis of polyphosphoinositides dependent on specific agents. Transformed cells were much less responsive to beta-adrenergic agonists in rising cAMP than normal cells. They are instead much more sensitive to muscarinic receptor agonists, inducing a rapid intracellular accumulation of inositol phosphates. These results suggest that the functional alteration of the cell membrane caused by the product of the point mutated H-ras oncogene concerns in 3T3 fibroblasts both inhibitory and stimulatory effects, respectively on adenylate cyclase and phosphoinositide-phosphodiesterase.
Chiarugi
V
V
Porciatti
F
F
Pasquali
F
F
Bruni
P
P
D000262:Adenylyl Cyclases / Q000032:analysis*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D002478:Cells, Cultured; D019204:GTP-Binding Proteins / Q000502:physiology; D006868:Hydrolysis; D051379:Mice; D009857:Oncogenes; D010716:Phosphatidylinositols / Q000378:metabolism*; D011976:Receptors, Muscarinic / Q000502:physiology*
D000318:Adrenergic beta-Agonists; D010716:Phosphatidylinositols; D011976:Receptors, Muscarinic; D019204:GTP-Binding Proteins; D000262:Adenylyl Cyclases