Cellular oncogenes, growth factors, and cellular growth control.
In this article we relate the functioning of oncogenes, particularly myc and ras, to current ideas regarding regulation of mammalian cell growth by growth factors. Assuming the genetic basis of transformation to be alterations of several proto-oncogenes, the mechanisms by which transformation could diminish growth control are numerous. The oncogene could interact with a growth factor in several ways. Mutations could alter the quantity of an oncogene's product or its quality through primary structure or covalent modifications such as phosphorylations. Oncogenes could code for a receptor for a growth factor. Various alterations parallel to the above set could then affect growth factor function via receptor changes (including abolished requirement for the factor). Some oncogenes might operate during the chain of intracellular events that must follow growth stimulation. Introduction of such an oncogene (e.g., the coding region for a DNA virus T antigen) would bypass requirements for both growth factors and receptors. Various observations regarding the oncogenes, cell cycle-timed events, and growth factors have been presented in a way we hope will suggest experiments designed to provide a basis for understanding growth regulation at the genetic, biochemical, and cellular levels in normal cells and tumorigenic cells, which have deranged growth regulation.
D002453:Cell Cycle; D002455:Cell Division; D004261:DNA Replication; D006133:Growth Substances / Q000502:physiology*; D007399:Interphase; D009857:Oncogenes
D006133:Growth Substances