The oncogenic forms of N-ras or H-ras prevent skeletal myoblast differentiation.

• DOI: 10.1128/mcb.7.6.2104
• Publication Date: 2015-09-30T19:41:54Z
• Authors: E N Olson; G Spizz; M A Tainsky
• Keywords: 0303 health sciences; Muscles; Glyceraldehyde-3-Phosphate Dehydrogenases; Cell Differentiation; Oncogenes; Cell Line; Mice; 03 medical and health sciences; Gene Expression Regulation; Genes; Proto-Oncogenes; Animals; Receptors, Cholinergic; RNA, Messenger; Growth Substances; Creatine Kinase; Cell Division

Differentiation of skeletal muscle involves withdrawal myoblasts from the cell cycle, fusion to form myotubes, and coordinate expression a variety muscle-specific gene products. Fibroblast growth factor type beta transforming specifically inhibit myogenesis; however, transmembrane signaling pathways responsible for suppression differentiation by these factors remain elusive. Because ras proteins have been implicated in transduction signals across plasma membrane, we used DNA-mediated transfer investigate potential involvement this family regulatory control myogenesis. Transfection mouse line C2 with oncogenic forms H-ras or N-ras completely suppressed both myoblast induction products nicotinic acetylcholine receptor creatine kinase. Inhibition activated genes occurred at level mRNA accumulation. In contrast, proto-oncogenic had no apparent effects on ability cells differentiate. Myoblasts transfected exhibited normal properties ceased proliferating absence mitogens, indicating that inhibited through mechanism independent proliferation. These results demonstrate mimic inhibitory fibroblast myogenic suggest each regulators myogenesis may operate common intracellular pathway.