Mutations and elevated levels of the p53 tumor suppressor protein have been reported in Burkitt's lymphomas (BL). We investigated whether elevated levels of the mutant p53 protein can be due to transcriptional or posttranscriptional mechanisms. In surveying a series of B-lymphoid cell lines, we found that a high level of the p53 protein tended to reflect high steady-state levels of p53 mRNA. p53 mRNA exhibited high stability in all of the cells tested. Cycloheximide treatment of the cells showed that the low level of p53 mRNA in non-BL lymphoid cells can not be attributed to posttranscriptional regulation by a labile protein. Nuclear run-on experiments revealed that the transcription rate of the p53 gene is about four times higher in some high p53-expressing BL cell lines as compared in low p53-expressing lymphoid cell lines. Our data suggest that an increase in the rate of transcription of the p53 gene is one of the mechanisms that contribute in elevated levels of mutant p53 protein observed in many tumor cells.
|Number of pages||6|
|Publication status||Published - Apr 1 1996|
ASJC Scopus subject areas
- Cancer Research