c-myc mRNA levels in the cell cycle change in mouse erythroleukemia cells following inducer treatment.
- 1 August 1985
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 82 (16) , 5323-5327
- https://doi.org/10.1073/pnas.82.16.5323
Abstract
Several lines of evidence suggest that the c-myc protooncogene is involved in some aspect of cell division in mammalian cells. Changes were investigated in the expression of c-myc mRNA in mouse erythroleukemia cells during chemically induced terminal erythroid differentiation. In vitro induction of erythroleukemia cell differentiation results in a switch from cells with unlimited proliferative capacity to cells that undergo a small number of terminal cell divisions. The level of c-myc mRNA changes rapidly following treatment with inducing agents. After a very rapid decline the mRNA is restored to pretreatment levels and then declines again. The level of c-myc mRNA was measured with respect to position in the cell cycle. Prior to inducer treatment the level of c-myc mRNA is relatively constant throughout the cell cycle. When the mRNA is restored following treatment with hypoxanthine or hexamethylenebisacetamide, it is found primarily in cells in the G1 phase. Treatment with inducers of differentiation leads to a change in the cell cycle regulation of c-myc mRNA. This change may be involved in the altered profiferative capacity of the cells that occurs during terminal differentiation.Keywords
This publication has 37 references indexed in Scilit:
- c-myc oncogene protein synthesis is independent of the cell cycle in human and avian cellsNature, 1985
- Stimulation of 3T3 cells induces transcription of the c-fos proto-oncogeneNature, 1984
- Transcriptional activation of the translocated c-myc oncogene in mouse plasmacytomas: Similar RNA levels in tumor and proliferating normal cellsCell, 1984
- Cell-specific regulation of the c-myc gene by lymphocyte mitogens and platelet-derived growth factorCell, 1983
- Identification of the c- myc Oncogene Product in Normal and Malignant B CellsScience, 1983
- Translocation, breakage and truncated transcripts of c-myc oncogene in murine plasmacytomasNature, 1983
- A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogeneNature, 1982
- Mechanism of activation of a human oncogeneNature, 1982
- Commitment to erythroid differentiation by friend erythroleukemia cells: a stochastic analysisCell, 1976
- Competition hybridization by “pre-saturation” of HeLa cell DNAJournal of Molecular Biology, 1969