The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional

Feng Zhou, Rheem D. Medh, Weiping Zhang, Naseem H. Ansari, E. Brad Thompson

    Research output: Contribution to journalArticle

    4 Scopus citations

    Abstract

    Because of their ability to induce lymphoid cell apoptosis, glucocorticoids have been used for decades to treat certain human leukemias and lymphomas. Studies presented in this paper complement our previous work demonstrating that sustained induction of the proto-oncogene c-jun plays a crucial role in the glucocorticoid-induced apoptotic pathway in CEM cells, human leukemic lymphoblasts. Results from measurements of c-jun mRNA half-life with RNase protection assays and of transcription by nuclear run-on assays indicate that, in the dexamethasone-sensitive cloned CEM-C7 cells, c-jun is induced at the transcriptional level. Consideration of time-course, however, suggested that this might be a secondary or possibly a delayed primary response. Use of cycloheximide to block protein synthesis strongly induced c-jun mRNA, suggesting that there had been relief from a labile protein repressor of transcription. Comparing the level of induction by cycloheximide with that of dexamethasone indicated that the two did not induce by an identical mechanism. The high induction by cycloheximide obscured simple interpretation of elevated c-jun mRNA levels after concomitant administration of cycloheximide and dexamethasone. This was resolved by nuclear run-on experiments, which showed that the dexamethasone induction of c-jun mRNA in this system does require protein synthesis.

    Original languageEnglish (US)
    Pages (from-to)91-99
    Number of pages9
    JournalJournal of Steroid Biochemistry and Molecular Biology
    Volume75
    Issue number2-3
    DOIs
    StatePublished - Dec 15 2000

    Keywords

    • Apoptosis
    • CEM cells
    • Glucocorticoids
    • Lymphoid
    • c-jun Gene regulation

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Biochemistry
    • Molecular Medicine
    • Molecular Biology
    • Endocrinology
    • Clinical Biochemistry
    • Cell Biology

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