Suppression of carcinogenesis by retinoids: interactions with peptide growth factors and their receptors as a key mechanism.
To understand the molecular mechanism of action of retinoids in control of differentiation and carcinogenesis, it is now necessary to consider the interactions of retinoids with oncogenes, as well as with peptide growth factors and their receptors. Experimental studies in these areas are described. In particular, it is shown that retinoic acid inhibits the proliferative effects of transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) on fibroblasts that have been transfected with the c-myc oncogene. The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene.
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D004815:Epidermal Growth Factor / Q000037:antagonists & inhibitors; D066246:ErbB Receptors / Q000187:drug effects / Q000502:physiology; D006131:Growth Inhibitors; D006133:Growth Substances / Q000502:physiology*; D006801:Humans; D009374:Neoplasms, Experimental / Q000517:prevention & control*; D009857:Oncogenes / Q000187:drug effects*; D010455:Peptides / Q000037:antagonists & inhibitors; D010982:Platelet-Derived Growth Factor / Q000037:antagonists & inhibitors; D012176:Retinoids / Q000494:pharmacology* / Q000627:therapeutic use; D015291:Transforming Growth Factors
D006131:Growth Inhibitors; D006133:Growth Substances; D010455:Peptides; D010982:Platelet-Derived Growth Factor; D012176:Retinoids; D004815:Epidermal Growth Factor; D015291:Transforming Growth Factors; D066246:ErbB Receptors