Post-transcriptional control of myc and p53 expression during differentiation of the embryonal carcinoma cell line F9.

摘要: Teratocarcinoma cells provide us with a model system for the study of differentiation and development1–3. One best characterized cell lines, embryonal carcinoma stem line F9, differentiates after treatment retinoic acid (RA) dibutyryl cyclic AMP into parietal endoderm4. This process is accompanied by induction several genes, example, those encoding collagen IV, plasminogen activator intermediate filaments like laminin4–6. In contrast, marked reduction stable messenger RNA has been observed gene p53 c-myc7,8. Both cellular oncogenes seem to be involved in regulation proliferation neoplastic transformation8–12. For growth-arrested 3T3 fibroblasts, growth-factor-induced changes myc are controlled at level transcription13. F9 which able change from tumorigenic state non-dividing, non-tumorigenic endodermal cells5. The latter enabled genes same different stages growth, tumorigenicity differentiation. Here we report that down-regulation during irreversible occurs post-transcriptional level. Using an vitro nuclear transcription assay14, found polymerase II density on both remains constant agreement this interpretation, detected as transcripts differentiated cyclo-heximide. regulatory mechanisms controlling stability follow kinetics. Whereas seems early event occurring within first 24 h, later stage (two three days), possibly consequence cycle changes.