Abstract
F9 embryonal carcinoma cells express high levels of a 53,000-molecular-weight cellular tumor antigen called p53. When F9 cell cultures are treated with retinoic acid and dibutyryl adenosine 3',5'-phosphate, they differentiate, predominantly into endoderm-like cells. This differentiation is accompanied by a marked decrease in the levels of p53. The mechanism(s) responsible for this decline in the level of p53 in differentiated cells was investigated. The results demonstrate that the high levels of p53 in F9 cells relative to their differentiated progeny were not due to alterations in the stability or turnover of this protein. Rather, the regulation during differentiation involved a marked decrease in the amount of in vitro translatable p53 mRNA detected in the differentiated cell cultures. This mechanism is unlike the one operating during the simian virus 40 infection or transformation, where the increased levels of p53 are largely due to the increased stability of the p53 protein.
MeSH Terms
Animals
Bucladesine/pharmacology
Cell Differentiation
Cell Transformation, Viral
Cells, Cultured
Fibroblasts
Mice
Mice, Inbred BALB C
Phosphoproteins/genetics,metabolism
RNA, Messenger
Simian virus 40
Teratoma
Tretinoin/pharmacology
Tumor Suppressor Protein p53
Chemicals
Phosphoproteins
RNA, Messenger
Tumor Suppressor Protein p53
Tretinoin
Bucladesine
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Oren M
Reich N C
Levine A J
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22 references, click to expand
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