Post-transcriptional control of myc and p53 expression during differentiation of the embryonal carcinoma cell line F9 - PubMed (original) (raw)
. 1985 Oct;317(6038):636-9.
doi: 10.1038/317636a0.
- PMID: 2414665
- DOI: 10.1038/317636a0
Post-transcriptional control of myc and p53 expression during differentiation of the embryonal carcinoma cell line F9
C Dony et al. Nature. 1985 Oct.
Abstract
Teratocarcinoma cells provide us with a model system for the study of differentiation and development. One of the best characterized cell lines, the embryonal carcinoma stem cell line F9, differentiates after treatment with retinoic acid (RA) and dibutyryl cyclic AMP into parietal endoderm. This differentiation process is accompanied by the induction of several genes, for example, those encoding collagen IV, plasminogen activator and intermediate filaments like laminin. In contrast, a marked reduction of stable messenger RNA has been observed for the gene encoding p53 and for c-myc. Both cellular oncogenes seem to be involved in the regulation of cellular proliferation and neoplastic transformation. For growth-arrested 3T3 fibroblasts, growth-factor-induced changes of myc RNA are controlled at the level of transcription. In contrast, F9 cells provide a differentiation system in which cells are able to change from a tumorigenic state into non-dividing, non-tumorigenic endodermal cells. The latter process enabled us to study the regulation of myc and p53 genes in the same cells at different stages of growth, tumorigenicity and differentiation. Here we report that down-regulation of stable myc and p53 RNA during irreversible differentiation of F9 cells occurs at the post-transcriptional level. Using an in vitro nuclear transcription assay, we found that the polymerase II density on both genes remains constant during differentiation. In agreement with this interpretation, we detected myc RNA as stable transcripts in differentiated F9 cells after treatment of the cells with cycloheximide. The post-transcriptional regulatory mechanisms controlling p53 and myc stability follow different kinetics. Whereas the down-regulation of myc seems to be an early event of F9 differentiation occurring within the first 24 h, the post-transcriptional regulation of p53 occurs at a later stage (two to three days), possibly as a consequence of cell cycle changes.
Similar articles
- Lack of correlation between loss of anchorage-independent growth and levels of transformation-specific p53 protein in retinoic acid-treated F9 embryonal carcinoma cells.
Rodrigues M, Balicki D, Newrock KM, Mukherjee BB. Rodrigues M, et al. Exp Cell Res. 1985 Jan;156(1):22-30. doi: 10.1016/0014-4827(85)90258-7. Exp Cell Res. 1985. PMID: 2981174 - Molecular analysis of early growth-associated events during the differentiation of F9 cells into embryoid bodies.
Whitman MM, Shen YM, Soprano D, Soprano KJ. Whitman MM, et al. Cancer Res. 1990 Jun 1;50(11):3193-8. Cancer Res. 1990. PMID: 2139801 - Post-transcriptional regulation of the abundance of mRNAs encoding alpha-tubulin and a 94,000-dalton protein in teratocarcinoma-derived stem cells versus differentiated cells.
Howe CC, Lugg DK, Overton GC. Howe CC, et al. Mol Cell Biol. 1984 Nov;4(11):2428-36. doi: 10.1128/mcb.4.11.2428-2436.1984. Mol Cell Biol. 1984. PMID: 6513923 Free PMC article. - Differentiation primary response genes and proto-oncogenes as positive and negative regulators of terminal hematopoietic cell differentiation.
Liebermann DA, Hoffman B. Liebermann DA, et al. Stem Cells. 1994 Jul;12(4):352-69. doi: 10.1002/stem.5530120402. Stem Cells. 1994. PMID: 7951003 Review. - Oncogene- and tumor-suppressor gene-related proteins in plants and fungi.
Loidl A, Loidl P. Loidl A, et al. Crit Rev Oncog. 1996;7(1-2):49-64. doi: 10.1615/critrevoncog.v7.i1-2.40. Crit Rev Oncog. 1996. PMID: 9109497 Review.
Cited by
- BAC transgenic mice provide evidence that p53 expression is highly regulated in vivo.
Chen L, Zhang GX, Zhou Y, Zhang CX, Xie YY, Xiang C, He XY, Zhang Q, Liu G. Chen L, et al. Cell Death Dis. 2015 Sep 17;6(9):e1878. doi: 10.1038/cddis.2015.224. Cell Death Dis. 2015. PMID: 26379189 Free PMC article. - MicroRNAs as Therapeutic Targets in Colitis and Colitis-Associated Cancer: Tiny Players With a Giant Impact.
Goel A. Goel A. Gastroenterology. 2015 Oct;149(4):859-61. doi: 10.1053/j.gastro.2015.08.041. Epub 2015 Aug 24. Gastroenterology. 2015. PMID: 26311277 Free PMC article. No abstract available. - Implications of miRNAs in Colorectal Cancer Chemoresistance.
Ju J. Ju J. Int Drug Discov. 2011 Feb-Mar;2011:2063. Int Drug Discov. 2011. PMID: 25750759 Free PMC article. - Beyond Thymidylate Synthase and Dihydrofolate Reductase: Impact of Non-coding microRNAs in Anticancer Chemoresistance.
Ju J. Ju J. Curr Enzym Inhib. 2012 Sep 1;8(2):118-123. doi: 10.2174/157340812800793228. Curr Enzym Inhib. 2012. PMID: 24683387 Free PMC article. - miRNA: the new frontier in cancer medicine.
Ju J, Jiang J, Fesler A. Ju J, et al. Future Med Chem. 2013 Jun;5(9):983-5. doi: 10.4155/fmc.13.74. Future Med Chem. 2013. PMID: 23734680 Free PMC article. No abstract available.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous