Interference with gene expression induces rapid apoptosis in p53-null T lymphoma cells

R. Ofir, L. C. Zhang, J. M. Adams

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Two p53-null T lymphoma cell lines proved to be highly sensitive to inhibition of gene expression. With either actinomycin D or cycloheximide, apoptosis commenced within 2 h, as indicated by loss of membrane integrity, degradation of certain proteins (including the phosphatase calcineurin) and DNA fragmentation. These effects were ablated by co-expression of Bcl-2 or co-incubation with the caspase inhibitor Z-VAD-fmk. These results suggest that the apoptotic machinery is in place in these cells but held in check by an unknown labile protein, which probably acts upstream of Bcl-2. Although cycloheximide can activate the JNK or p38 MAP kinases in some cells, neither was implicated here. However, disruption of phosphoinositide 3-kinase signaling may be involved, because the cells were also sensitive to wortmannin. The high sensitivity of the p53-null lymphoma cells to inhibitors of gene expression suggests that such inhibitors might prove useful in the cytotoxic therapy of certain tumors.

Original languageEnglish
Pages (from-to)1216-1221
Number of pages6
JournalCell Death and Differentiation
Issue number12
StatePublished - 1 Jan 1999


  • Apoptosis
  • Cycloheximide
  • Cytotoxic therapy
  • p53

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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