Selective inhibition of the anchorage-independent growth of myc -transfected fibroblasts by retinoic acid

• Published in: Nature (London) Vol. 315; no. 6016; pp. 237 - 239
• Main Authors: Roberts, Anita B, Roche, Nanette S, Sporn, Michael B
• Format: Journal Article
• Language: English
• Published: London Nature Publishing 01-01-1985
• Subjects: Animals; Biological and medical sciences; Cell Adhesion; Cell Division - drug effects; Cell physiology; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes; Cell Transformation, Viral; Cells, Cultured; Epidermal Growth Factor - pharmacology; ErbB Receptors; Fundamental and applied biological sciences. Psychology; Growth Inhibitors; Mice; Molecular and cellular biology; Oncogenes; Peptides - antagonists & inhibitors; Platelet-Derived Growth Factor - antagonists & inhibitors; Receptors, Cell Surface - drug effects; Transfection; Transforming Growth Factors; Tretinoin - pharmacology; Cell proliferation; Cell culture; Rat; Rodentia; Vertebrata; Suspension culture; Mammalia; Epidermal growth factor; Transfection; C-Onc gene; Dependence; Platelet growth factor; Inhibition; Fibroblast; Retinoic acid; Anchoring; Growth factor
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/315237a0

Fischer rat 3T3 (FR3T3) fibroblasts transfected with a cellular myc gene can be induced to grow and form colonies in soft agar by treatment either with epidermal growth factor (EGF) alone or with the combination of platelet-derived growth factor (PDGF) and type-beta transforming growth factor (TGF-beta). We now show that induction of anchorage-independent growth by each of these sets of growth factors involves different cellular pathways which can be distinguished by their sensitivity to retinoic acid. Colony formation induced by the combined action of PDGF and TGF-beta is 100-fold more sensitive to inhibition by retinoic acid than is colony formation induced by treatment of the myc-transfected cells with EGF. Moreover, retinoic acid (10(-8) M) is inhibitory for colony growth whenever TGF-beta is present, regardless of whether the effects of TGF-beta are stimulatory, as occurs in the presence of PDGF, or inhibitory, as found in the presence of EGF.