Bcl-2 inhibits T-cell-mediated cytolysis of a leukemia cell line |
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Authors: | T Torigoe JA Millan S Takayama R Taichman T Miyashita JC Reed |
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Affiliation: | Oncogene & Tumor Suppressor Gene Program, La Jolla Cancer Research Foundation, California 92037. |
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Abstract: | The bcl-2 gene becomes dysregulated in its expression in a wide variety of human cancers and has been shown to block both spontaneous and drug-induced cell death, thus conferring a selective survival advantage on malignant cells. The biochemical mechanism by which bcl-2 promotes cell survival remains enigmatic but appears to involve a downstream event in an evolutionarily conserved cell death pathway. Here we report that gene transfer-mediated increases in Bcl-2 protein levels in the human leukemia line Jurkat render these cells more resistant to induction of DNA fragmentation and cytolysis by a cloned T-cell. The killing mechanism used by these particular T-cells was consistent with apoptosis, as opposed to necrosis, in that DNA degradation occurred as a prelysis event. The findings raise the possibility that dysregulation of bcl-2 gene expression could play a role in the avoidance of immune surveillance mechanisms by cancer cells. |
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